*Shave Biopsy Negatively Affects Melanoma Treatment Decision Making Posted Wednesday, March 29, 2006 by arjuna
http://www.docguide.com/news/content.nsf/news/852571020057CCF68525713E004FB914

By Crystal Phend SAN DIEGO, C.A. -- March 27, 2006 -- Although shave biopsies are often used in an attempt to remove the entire melanoma, excisional biopsy should be the preferred biopsy method, researchers said here at the annual meeting of the Society of Surgical Oncology (SSO). "The standard should be excisional biopsy," said presenting author Richard L. White, Jr., MD, chief of the division of surgical oncology, Carolinas Medical Center, Charlotte, North Carolina, United States. "If you are going to do a shave biopsy, you need to make it a much thicker biopsy." Dr. White and colleagues reviewed 223 cases of primary melanoma with known method of biopsy. Margins from the biopsies were either indicated on the pathology report or reviewed from specimen slides. Fifty-one of the patients had excisional biopsy while 44 had a punch biopsy and 128 had a shave biopsy. Although shave biopsy was by far the most common method, it also had the highest percentage of deep (more than 1 mm) positive margins at 22%, and a high percentage of positive margins overall at 50%. "The presence of positive margins and in particular the presence of deep positive margins, in such a large percentage of the shave biopsy specimens compromises the ability of this technique to properly stage patients," Dr. White said. This could compromise appropriate treatment recommendations as well, he added. Comparatively, excisional biopsy had the lowest number of positive margins (16%) and no deep positive margins. Punch biopsy also had no deep positive margins but had the highest rate of positive margins (68%). "The presence of tumor at the margin of punch biopsies is an expected result, since this method is often used to diagnose lesions with a large diameter," Dr. White explained. Mean biopsy thickness was 3.19 mm for excisional biopsy, 3.58 mm for punch biopsy, and 1.41 mm for shave biopsy. The differences between methods were significant as were those between punch and shave biopsy. Dr. White added that the average depth for shave biopsy was "much, much too thin." [Presentation title: Method of Biopsy and Incidence of Positive Margins in Primary Melanoma. Poster 83]
Comments (10576)

Mutations In The BRAF Gene Predict Sensitivity To A Novel Class Of Cancer Drugs Posted Wednesday, November 9, 2005 by arjuna
Source: Memorial Sloan-Kettering Cancer Center
Date: 2005-11-07
URL: http://www.sciencedaily.com/releases/2005/11/051107075734.htm

A team of researchers led by scientists at Memorial Sloan-Kettering Cancer Center have discovered that a new class of drugs -- now in early stage clinical trials -- work best in patients with mutations in the BRAF gene. BRAF is a protein that plays a central role in the growth and survival of cancer cells and is mutated in the majority of patients with melanoma and in a minority of patients with colon, breast, and lung cancers. The findings, available in an advance online publication of Nature, represent a potential targeted therapy tailored for patients whose tumors contain this mutation.

The researchers found that drugs that inhibit a protein called MEK selectively inhibited the growth of cancer cells lines and tumors that have a mutated BRAF gene. One of these drugs, PD0325901 (developed by Pfizer Research and Development), is now being tested in clinical trials of patients with melanoma, colon, breast, and lung cancers. In addition, by re-analyzing the data on more than 42,000 compounds tested by the National Cancer Institute against a panel of 60 cancer cell lines, the investigators were able to identify a small number of other compounds that also selectively inhibit tumors that have the BRAF mutation. While the mechanism of action of some of these compounds has yet to be determined, several of the most effective compounds were also inhibitors of the MEK protein.

"We find that all tumors with the BRAF mutation and some with the RAS mutation are sensitive to drugs that inhibit MEK," explained Dr. Neal Rosen, Professor of Medicine and a member and laboratory head in the Molecular Pharmacology and Chemistry Program at Memorial Sloan-Kettering and the study's senior author. "Translating these findings into a strategy for treating patients whose tumors are dependent upon this specific genetic change is the next step, and such clinical trials are now ongoing."

"The BRAF mutation was first identified by a consortium of investigators searching for proteins that are frequently mutated in human cancer," said Dr. David Solit, the study's first author and a medical oncologist at Memorial Sloan-Kettering who is also a member of Dr. Rosen's laboratory. This project, an outgrowth of the Human Genome Project, called the Cancer Genome Project, has the goal of identifying the causative mutations that cause human cancers.

"This represents what we believe will be the first of a series of new drugs that specifically target cancer cells that contain mutations identified by the Cancer Genome sequencing effort," said Dr. Solit. "The hope is that these new targeted therapies will be more effective and less toxic than traditional chemotherapies."

The study's other researchers were Christine A. Pratilas, Ayana Sawai, Andrea Basso, Qing Ye, Jose M. Lobo, and Yuhong She, all of Memorial Sloan-Kettering; Drs. Levi A.Galloway, Gad Getz, Todd R. Golub, and William R. Sellers of Dana-Farber Cancer Institute and Broad Institute of MIT and Harvard; Dr. Iman Osman of New York University Medical College; and Dr. Judith Sebolt-Leopold of Pfizer Global Research and Development.


###

This work was supported by grants from the National Institutes of Health, the William H. Goodwin and Alice Goodwin Foundation for Cancer Research, the Memorial Sloan-Kettering Cancer Center Experimental Therapeutics Center, the Waxman Foundation, the Howard Hughes Medical Institute, Golfers Against Cancer, and the American Society of Clinical Oncology.

Memorial Sloan-Kettering Cancer Center is the world's oldest and largest institution devoted to prevention, patient care, research, and education in cancer. Our scientists and clinicians generate innovative approaches to better understand, diagnose, and treat cancer. Our specialists are leaders in biomedical research and in translating the latest research to advance the standard of cancer care worldwide. For more information, go to www.mskcc.org Comments (5358)

Enzyme Might Be Culprit in Skin Cancer's Spread Posted Friday, November 4, 2005 by arjuna
http://www.healthday.com/view.cfm?id=528900

Helps tumor cells move around body; finding could lead to therapies,
experts say

**By Alan Mozes*
/HealthDay Reporter/*

THURSDAY, Nov. 3 (HealthDay News) -- Overactivity of a key enzyme found
in skin cancer cells appears to play a prominent role in triggering the
aggressive spread of the disease, a new study suggests.

The enzyme -- known as focal adhesion kinase (FAK) -- is present in
every cell of the human body, and is critical to the healthy promotion
of many cellular activities.

However, this enzyme's unhelpful behavior within malignant melanoma
cells is now gaining scientific attention.

The researchers noted that the FAK enzyme has previously been found to
be overactive across a wide range of aggressive malignancies, including
eye, prostate, thyroid, colorectal, ovarian and oral cancers.

The current work raises the hope that a better understanding of FAK's
role may ultimately lead to the development of new early stage
treatments that hone in on the enzyme and halt its ability to promote
the migration of malignant cells throughout the body.

Such metastasizing of a localized and curable cancer can make melanoma
much more difficult to treat and control -- even leading to an otherwise
preventable death, the study authors said.

"FAK has been shown for a lot of different types of cancers to play a
role in the tumor cells' ability to move within the body and set up
shop, so I think targeting it to reduce the risk of melanoma
metastasizing is a very exciting idea," said study author Angela R.
Hess, a research scientist at Children's Memorial Research Center in the
Feinberg School of Medicine at Northwestern University. "But this is in
its very early infancy as a therapy."

The American Cancer Society notes that the incidence of melanoma in the
United States has tripled over the past 50 years -- nearly doubling in
the last decade alone. Its estimates indicate that nearly 60,000 new
cases of melanoma will be diagnosed in 2005, resulting in about 7,770
deaths.

Hess and her team conducted lab analyses on samples of both aggressive
and non-aggressive human skin and eye cancer cells.

In the November issue of /Cancer Research/, the authors report that
cancer cell aggressiveness appeared to be a function not so much of
elevated FAK levels, but rather of elevated FAK activity.

"The important thing is that the cancer cell, in and of itself, has a
very deregulated system so the FAK protein can make the cell go wild
when it's inappropriately active," Hess noted.

Such increased enzyme activity was associated with an overall increase
in the melanoma cancer cell's ability to move beyond the borders of the
tumor and invade healthy areas of the body, the researchers said.

In addition, increased FAK expression was associated with an increase in
so-called tumor cell plasticity, in which a cancerous cell improves its
chances of spreading by forming its own vascular network to masquerade
as an otherwise healthy cell.

The researchers further found that when they blocked FAK activity in
certain aggressive cancer cells, the diseased cells displayed a 70
percent drop in their ability to migrate, and a 60 percent drop in their
ability to invade tissue outside the tumor area. Tumor cell plasticity
was also observed to be halted when FAK activity was neutralized.

The authors concluded that FAK appears to play a kind of gatekeeper role
in the opening up of pathways that promote the spread of cancer cells
throughout the body. And while they acknowledged that the signaling
mechanism that FAK activity initiates is not yet fully understood, they
noted that a selective disruption of FAK behavior might slow cancer down.

"Basically the major point is that we're trying to understand what
enables melanoma tumor cells to move out from the initial primary tumor
to another site in the body, because once that happens melanoma tends to
become very difficult to treat and the five-year survival rate drops
considerably," Hess said.

"So this is just an idea," she stressed. "And it takes a while to
actually produce a drug. But potentially, at some point in the future,
we can somehow focus on that specific FAK protein to stop the melanoma
from moving."

A similarly cautious tone was sounded by Dr. Jean-Claude Bystryn, a
professor of dermatology at New York University School of Medicine, and
former head of the melanoma program and vaccine clinic at New York
University Medical Center in New York City.

"Trying to find ways to slow the progression or spread of cancer is
clearly a very major challenge," said Bystryn. "But at this stage, it's
difficult to tell what the best approach is going to be because there
are multiple mechanisms that are involved in the spread of cancer."

"So these molecules of FAK may be involved," he added, "and there's
always hope that interfering with one of these mechanisms will be
effective in slowing the spread. So from my perspective, it's worthwhile
exploring --assuming that you know that we're not really sure if this is
going to work or not."

*More information*

For more on melanoma, check with the American Cancer Society
.



SOURCES: Angela R. Hess, research scientist, Children's Memorial
Research Center, Feinberg School of Medicine, Northwestern University,
Chicago; Jean-Claude Bystryn, professor, dermatology, New York
University School of Medicine, and former head, melanoma program and
vaccine clinic at New York University Medical Center, New York City;
November 2005 /Cancer Research/

Cancer Control Journal at Moffitt Cancer Center Posted Friday, November 4, 2005 by arjuna

October 2005

http://www.moffitt.usf.edu/pubs/ccj/index.htm

The October, 2005 issue of "Cancer Control", Journal of the Moffitt Cancer Center, is dedicated to melanoma and freely available in pdf. format online. Comments (9830)

Key to why melanoma is so potent Posted Sunday, September 4, 2005 by arjuna
http://news.bbc.co.uk/1/hi/health/4207340.stm
BBC NEWS

* Scientists have discovered why a form of skin cancer called melanoma
can be so malignant. *

If not caught early the disease can spread through the body with an
efficiency few other tumours possess.

Latest research suggests that, unlike other cancer cells, melanoma does
not have to learn how to spread - it has that ability innately.

The research, by Whitehead Institute for Biomedical Research in the US,
is published in Nature Genetics.


*Certain embryonic genes normally involved in transferring cells from
one part of the body to another are also involved in enabling cancer
cells to spread *
Professor Robert Weinberg,
Lead researcher

Lead researcher Professor Robert Weinberg said: "Other cancers need to
learn how to spread, but not melanoma.

"Now, for the first time, we understand the genetic mechanism
responsible for this."

The spread of disease to an unconnected body part - known as metastasis
- is a highly inefficient, multi-step process that requires cancer cells
to jump through many hoops.

* Slug gene *

The cells first must invade a nearby tissue, then make their way into
the blood or lymphatic vessels.

Next they must migrate through the bloodstream to a distant site, exit
the bloodstream, and establish new colonies.

Researchers have wondered why melanoma in particular is able to do this
not only more efficiently than other cancers, but at a far earlier stage.

The latest study shows that as melanocytes - cells that protect the skin
from sun damage by producing pigmentation - morph into cancer cells,
they immediately reawaken a dormant cellular process that lets them
travel swiftly throughout the body.

Central to this reawakened process is a gene called Slug which plays a
key role in allowing cells to travel around the developing embryo in the
womb.

Normally the gene is shut off in adult tissues, but the researchers
found that when skin cells become malignant they reactivate Slug, and
thus immediately acquire the ability to spread.

* Injected cells *

The researchers injected cancer-causing genes into normal human cells
and then injected the resulting tumours under the skin of mice.

Mice injected with breast or connective tissue cancer cells developed
tumours - but these did not spread.


* It is also important to remember that the vast majority of melanomas
are caused by UV damage from excess sun exposure *
Dr Julie Sharp,
Cancer Research UK

But those injected with melanoma cells immediately developed invasive
tumours throughout their body.

Detailed analysis showed that Slug was expressed in the melanoma cells.

When the gene was knocked out in melanoma cells, the cancer was unable
to spread when introduced into a mouse.

Professor Weinberg said: "This work is a demonstration of the notion
that certain embryonic genes normally involved in transferring cells
from one part of the body to another are also involved in enabling
cancer cells to spread."

The same team last year showed a similar embryonic gene, Twist, played a
role in the spread of certain forms of breast cancer.

Dr Julie Sharp, senior cancer information officer at Cancer Research UK,
said: "If scientists can target treatments to block the Slug gene, they
might be able to prevent cancer spread and improve survival from this
disease in the future," she said.

"It is also important to remember that the vast majority of melanomas
are caused by UV damage from excess sun exposure."

Comments (18731)

Why sunshine poses a greater cancer risk to readheads Posted Friday, September 2, 2005 by arjuna
http://www.timesonline.co.uk/article/0,,2-1754923,00.html

August 29, 2005

By Nigel Hawkes, Health Editor

REDHEADS run a greater risk of skin cancer from exposure to the sun than people with darker hair.

The reason, according to a talk given yesterday at the American Chemical Society’s meeting in Washington, is that small differences in the chemistry of the skin pigments in people with different coloured hair affects the production of cancer-causing agents when the skin is exposed to ultra-violet light.

The risk of skin cancer is about two to four times higher for redheads and blonds than for those with dark hair. In 1995 there were 5,626 new cases of melanoma — the most dangerous form of skin cancer — in Britain, but by 2000 this had risen to 6,967. Each year about 1,700 people die from melanoma, the third most common cancer among people aged 15 to 39.

A group led by Professor John Simon of Duke University, North Carolina, isolated the melanin-containing structures, called melanosomes, from human hair and then measured the oxidation potentials of the different melanins. Oxidation potentials are a measure of how likely chemicals are to create highly active oxygen radicals by taking up electrons. Oxygen radicals, in turn, are known to be damaging to DNA, and DNA damage is the trigger for cancer. So if the team could find differences in the oxidation potentials of the melanins, it could explain differences in skin cancer risk.

To measure the potentials the team subjected the melanins to precisely tuned laser light in the right region of the ultraviolet spectrum. The results reported yesterday showed that black pigments were indeed less likely to produce oxygen radicals, and red pigments more likely to.

While the finding may explain the higher risk of redheads, it does not offer them any way to reduce it. They will simply have to take greater care not to become sunburnt.

If the red-haired gene carries this risk, why has it not died out? The answer is that it is indeed much more common in northerly climes, where it may also offer an advantage. One theory is that the red-haired melanins help the skin to create vitamin D in colder climates, thus reducing the risk of diseases such as rickets.

An alternative explanation is that the pale skin that often goes with red and strawberry blonde hair is so attractive that it helps women who possess it to get mates.


Comments (13455)

The good sun? Posted Friday, September 2, 2005 by arjuna
http://www.boston.com/news/globe/health_science/articles/2005/08/29/the_good_sun?mode=PF

Skin cancer is as deadly as ever, but now some doctors wonder if avoiding all rays is the answer

By Brian Kladko, Globe Correspondent | August 29, 2005

All it takes is a trip to the South Boston waterfront to see that dermatologists have a long way to go in their campaign against melanoma, the deadliest form of skin cancer.

Among those recently basking in the hazy sunshine at Carson Beach were Karen and Ed Crowley, both 46, of Dorchester. They had been lying out for more than two hours without sunscreen because they forgot to pack it.

''What are you going to do?" said a bare-chested Ed, a construction worker who said he also takes his shirt off at job sites, as long as temperatures allow for it. ''You want to walk through life afraid of everything?"

A few feet away, Lynn Krause was working on her tan, too. She deliberately shunned the sunscreen.

''If you're out to get a tan, then there's no point in using it," said the 34-year-old South End resident. As for skin cancer, she said, ''Whatever happens, happens."

Whether they're lying on Carson Beach, fishing in Boston Harbor, or skiing on Mount Snow, Americans still blithely defy dermatologists' warnings that melanoma is a growing menace, caused mostly by people's bad habits.

Named for the pigment-producing skin cells, called melanocytes, where the disease takes root, melanoma will afflict another 60,000 Americans this year and kill about 8,000. Unlike the two most common forms of skin cancer, melanoma can spread to other parts of the body, making it far more lethal.

But some skeptics question the very notion that melanoma is on the rise. And there's a growing disagreement about the dangers of moderate sun exposure. Some doctors argue that 10 to 15 minutes per day of sunshine, without sunscreen, will prevent far more cancers than it will cause. Others suggest getting enough rays to turn the skin pink a few times a week.

''We just need to be sensible about it," said Kathleen Egan, an epidemiologist at Vanderbilt University School of Medicine. ''Common sense says that you don't want to overdo it in the sun, and that you should let your own susceptibility to the sun be the arbiter."

The claim that some sun could help the body ward off cancer, or better cope with it, isn't so new -- 25 years ago, researchers noted that cancer rates were higher in northern parts of the United States, where people get less sun exposure. (That's not true for melanoma -- it's more prevalent in Texas than Minnesota.) But the notion of healthy sunshine seems to be gaining momentum.

One study of 900 men in California found that men with darker tans had half the risk of advanced prostate cancer. Another study, looking at 6,000 people in Denmark and Sweden, found that people with a reported history of sunburns and sunbathing were less likely to get the disease.

Perhaps the most provocative finding came from Marianne Berwick, an epidemiologist at the University of New Mexico. In a study of 650 melanoma patients in Connecticut, she found that people who reported more sun exposure over their lifetimes had a better chance of surviving the disease. In other words, the same sunlight that could be a risk factor for melanoma could also increase the chances of beating it.

The most popular explanation for these findings is Vitamin D, which is manufactured by the skin when exposed to sunlight, assuming there's no sunscreen on it. People living in most of the United States -- including New England -- have a hard time making any Vitamin D during winter months and tend not to get the federal government's recommended daily intake from their diets, said Egan, who wrote an editorial accompanying Berwick's article. She also believes, like many other scientists, that the government's recommendations are too low.

But dermatologists maintain that sun, particularly intense sun, ''is the most avoidable risk factor that we know about," said Martin A. Weinstock, a Brown University dermatology professor and chairman of the American Cancer Society's skin cancer advisory group.

Weinstock said most of the Vitamin D-cancer research ''has been rather weak." Even if it proves true, he said, a concerned person would do better to get the nutrient by taking a pill or changing their diet (milk is fortified with it).

As the risks and benefits of sunshine become hopelessly muddled, a seemingly basic issue -- whether melanoma is on the rise -- has become just as cloudy.

Federal statistics show that US cases of the disease grew 2.4 percent a year between 1992 and 2002, making it the third-fastest growing cancer in the country.

But Dr. H. Gilbert Welch, a professor of medicine at Dartmouth Medical School, says most of that increase may be an illusion -- the result of more people being screened through programs like ''Melanoma Mondays," in which dermatologists offer free, on-site exams.

Welch, author of last year's ''Should I Be Tested for Cancer? Maybe Not and Here's Why," reported this month in the British Medical Journal that the average biopsy rate and diagnosis rate increased about 2.5 times between 1986 and 2001 for people 65 and older. But almost all that increase involved early-stage melanomas; the proportion of late-stage melanomas and the death rate stayed about the same. If the disease were truly on the rise, he said, the number of late stage cases and deaths should have risen, too.

''We're finding cases that we simply didn't find before," he said. ''But these aren't cases that are going to kill people."

Welch notes that many lesions diagnosed as melanoma won't become invasive. Also, doctors often disagree on which lesions are melanoma and which aren't, and in the face of that ambiguity, they err on the side of caution.

But just days before Welch's article appeared, the Journal of Clinical Oncology published an article saying childhood melanoma increased about 3 percent between 1973 and 2001. One of its authors, Dr. John Strouse, a pediatric oncologist at the Johns Hopkins University School of Medicine, believes at least some of that increase is real -- not just the result of more examinations.

Strouse suspects it's no coincidence 15- to 19-year-olds account for most of the increase, as it's those years when a nice tan takes on more importance. He also believes the increase in travel to sunny climes and the profusion of tanning salons has fueled the trend.

''I was down in Memphis for a meeting, and we were at a hotel there, and there was some high school dance at this hotel," he said. ''And all the girls were tan -- in February. And Memphis isn't that sunny. If you're tan in February, you're tanning indoors or you just went on vacation someplace."

Anecdotes like that make dermatologists wary of any research that muddles their message. In a country not known for moderation, they fear that people will disregard their warnings and, like the people on Carson Beach, soak up too much sun.

''Certainly the dermatology community has had this boring, 'no fun' story about staying out of the sun that's been going on really for 40 years or 50 years," said Dr. Barbara Gilchrest, chairwoman of the dermatology department at Boston University School of Medicine. But publicity about the recent findings of sun exposure's possible benefits, she said, ''was not a helpful public health message."

Signs of possible melanoma
# A mole that changes in size, shape, or color; has irregular edges or borders; is more than one color; is asymmetrical; oozes, bleeds, or is ulcerated so the underlying tissue shows through.
# A change in colored skin.
# Satellite, or new moles that grow near an existing one.

SOURCE: National Cancer Institute


Comments (2019)

Despite risks of melanoma, many still tan unprotected skin Posted Sunday, May 29, 2005 by arjuna


Wednesday, May 25, 2005
By Alana Semuels, Pittsburgh Post-Gazette

People take risks with their health every day. They go jogging without reflective gear. They eat fast food more than they should. They don't floss. And they love to lie out in the sun.

Doctors say that despite numerous warnings about the dangers of skin cancer, Americans still are willing to risk it through unprotected exposure to the sun, and that cavalier attitudes towards the sun could cause many more deaths from skin cancer in the coming years.

Marjorie Gross of Oakland and Wiley Master of Seven Fields are good illustrations of this. Gross did not heed the warnings of her physician father when she was young, and has battled skin cancer for the past 20 years. Master tried to do the good thing by introducing people to sunless tanning, but they just weren't interested.

Their dual experiences might help explain why the lifetime chances of getting melanoma, the deadliest form of skin cancer, are now about 1 in 65. By 2010, that risk will rise about 1 in 50, said Dr. John Kirkwood, director of the Melanoma Center at the University of Pittsburgh.

"That is an epidemic of untold proportions," he said.

Melanoma often hits people at a younger age than do other common types of cancers, affecting people in their 30s and 40s. More productive life years are lost to melanoma than to any cancers after pediatric and testicular cancers, Kirkwood said. And it's beginning to affect people who are even younger.

Some doctors even say that the incidence of melanoma in children, which previously was rare, is increasing. The two most common types of skin cancer, basal cell and squamous cell, are rarely deadly, so an increase in melanoma means more deaths caused by it.

Melanoma is dangerous because it is often not caught early enough. If diagnosed and treated early, it is not deadly. But if not caught, it can spread quickly to other layers of the skin and onto other organs in the body, at which point it's very difficult to treat.

Research suggests that sun has a negative effect on the immune system. It can damage the Langerhans cells in skin, which are essential in helping initiate immune response. With damaged cells, the immune system's response to foreign invaders is often delayed or subdued.

Skin cancer also preys on people with already weakened immune systems, said Dr. John Zitelli, a Pittsburgh doctor who is also on the medical board of the Skin Cancer Foundation.

Kidney transplant patients taking drugs to suppress their immune systems are susceptible to skin cancers.

Skin cancers are caused when UV light penetrates the skin and welds genes together to such a degree that the body cannot repair them.

While a bill has been introduced in the state legislature that would require anyone under 18 to get parental consent to use a tanning bed and would further regulate those establishments, no bill can stop teenagers or anyone else from lying out in the sun on a warm day.

Most doctors acknowledge that it is an individual's decision to tan, and that they can't force people to get smart about sun exposure. Despite all the warnings and horror stories about people dying from skin cancer, sun worshippers often don't think it will hapen to them.

Master opened a tanning salon in Seven Fields in January that offered spray-on tanning only. Within three months, he had to add tanning beds because his customers kept asking for them. He estimates he sells 100 tans in the beds per week, and only about three spray-on.

"I was very hesitant," to buy tanning beds, he said. "I wanted to be in the tanning business in a safer, smarter way."

Customers weren't interested.

Some chalk it up to the invincible feeling of youth.

Even when she was very young, Marjorie Gross, who is now in her 60s, knew that there was a high chance that she would get skin cancer. Her father was a doctor, and he pleaded with his fair-skinned, blue-eyed daughter to cover up.

"But I didn't," she said from the office of her skin cancer doctor. "I was concerned about getting a tan. I was a sun-worshipper."

She first got basal cell cancer 20 years ago, and has had surgeries about a dozen times since then to remove cancerous cells. She's also a breast cancer survivor, and takes medication that weakens her immune system, further making her susceptible to cancer.

"I'm paying the price now," she said. "It was a shock since you always think that it's not going to happen to you."

Comments (4953)

Even Kids Aren't Safe From Skin Cancer Posted Sunday, May 29, 2005 by arjuna

One bad burn can have dangerous consequences years later, experts say

By Dennis Thompson
HealthDay Reporter

SATURDAY, May 28 (HealthDay News)-- As the summer season kicks off with the long holiday weekend, kids across the United States are preparing for months of outdoor fun, from planning a tree fort to shopping for bikinis.

However, doctors warn that fun could have long-term consequences if kids don't properly protect themselves from the sun's rays.

Children who suffer just one severe, blistering sunburn have doubled their chances of getting skin cancer, according to medical experts.

What's more, a survey sponsored by the Centers for Disease Control and Prevention found that about 43 percent of white children under age 12 had at least one sunburn in the past year.

"You can recover from a sunburn, but there's still damage that has occurred," said Dr. Deborah S. Sarnoff, an assistant clinical professor of dermatology at New York University, a clinical consultant in the dermatology branch of the National Institutes of Health and an educational spokeswoman for the Skin Cancer Foundation. "Even though our skin cells turn over constantly, there's cumulative damage."

Skin cancer is the most common type of cancer in the United States, according to the National Cancer Institute. More than a million people are diagnosed with skin cancer each year, and current estimates say 40 percent to 50 percent of Americans who live to age 65 will have skin cancer at least once.

More than 90 percent of all skin cancers are caused by sun exposure -- specifically, exposure to the sun's ultraviolet radiation.

The sun is so directly linked to skin cancer that cases vary depending on the weather and sunlight of different regions, according to the American Cancer Society. For example, skin cancer is more common in Texas than in Minnesota, and the world's highest rates are found in South Africa and Australia.

Anyone can get skin cancer, but the risk is greatest for people who have fair skin that freckles easily. Folks with red or blond hair and blue or light-colored eyes should be particularly wary.

The two most common kinds of skin cancer are basal cell carcinoma and squamous cell carcinoma, with basal cell carcinoma accounting for more than 90 percent of all skin cancers in the United States. These cancers affect the two types of cells that make up the outer layers of the skin's surface; they're slow-growing and rarely spread to other parts of the body.

Less common but much more deadly is melanoma, a cancer that affects melanocytes, cells deep inside the epidermis that produce the coloring agent melanin.

Melanoma is much more likely to become malignant and spread to other parts of the body. Nearly 10,000 people died from skin cancer in 2004, and most of those died from melanoma, according to the CDC.

Most skin cancers appear after age 50, but the sun's damaging effects begin at an early age, according to the American Cancer Society. Protection should start in childhood to prevent skin cancer later in life.

It's a tough job, Sarnoff said. "Children's skin is thinner, more sensitive and delicate," she said. "It's much easier to get a sunburn as a kid than as an adult."

The best way to prevent skin cancer is to stay indoors when the sun's rays are at their strongest. Whenever possible, people should avoid exposure to the midday sun, roughly from 10 a.m. to 2 p.m. standard time or 11 a.m. to 3 p.m. daylight saving time.

If you must go out, you should shield as much of your body as possible from ultraviolet radiation, said Dr. Martin Weinstock, chairman of the American Cancer Society's skin cancer advisory group, a professor of dermatology at Brown University and chief of dermatology at the VA Medical Center in Providence, R.I.

"We have a slogan -- Slip, Slop, Slap," Weinstock said. "Slip on a shirt, slop on sunscreen and slap on a hat."

True coverage involves wearing as many clothes as possible, Sarnoff said. Sunblock is important, but it doesn't protect nearly well as clothing.

If your children are using sunblock, remember to reapply it every two hours if they are playing a sport or participating in some other activity that causes them to sweat, she said. And if they swim, they should reapply sunblock as soon as they come out of the water.

"We think teaching your kids proper sunblock use is as important as teaching them to brush their teeth or comb their hair," Sarnoff said. "It's basic grooming."

Parents also should remember that the sun is a risk even on cool spring or autumn days, Weinstock said.

"It's not the heat, it's the UV rays," he said. "Spring is a particularly important time to be careful. It may be cool out, and you may still need protection."

More information

To learn more about preventing skin cancer, visit the American Cancer Society.

SOURCES: Deborah S. Sarnoff, M.D., assistant clinical professor, dermatology, New York University, clinical consultant, dermatology, National Institutes of Health, Bethesda, Md., and spokeswoman, Skin Cancer Foundation, New York City; Martin Weinstock, M.D., chairman, Skin Cancer Advisory Group, American Cancer Society, professor, dermatology, Brown University, Providence, R.I., and chief, dermatology, VA
Comments (1552)

Metro schools shine spotlight on early lessons in sun safety Posted Sunday, May 29, 2005 by arjuna
Classes show kids how to prevent skin cancer by minimizing harmful sun exposure.

Sunday, May 29, 2005 By Karen Bouffard / The Detroit News

LIVONIA -- Eight-year-old Andrea Hall and her sister, Laura, 5, squiggle
and squirm when their mom applies sunscreen.

But as the summer outdoor season kicks off, Ginny Hall of Livonia is
determined to protect her children from the sun's ultraviolet rays,
which can cause skin cancer.

"It's hard for them to stand still; they especially don't want it on
their face," Ginny Hall said. "They don't want to stop playing to have
it put on. But my husband wears it, I wear it; it's just a ritual.

"Bottom line: We know it's what's best for them."

The girls attend Garfield Elementary in Livonia, one of 10 schools to
receive "Sun Safety" grants through the Michigan Parent Teacher Student
Association. The grants originated through the federal Centers for
Disease Control and Prevention and the American Cancer Society.

The CDC and the society have made fighting skin cancer a national
priority. It is now the most common form of cancer in the United States.
The society last year estimated 1.6 million new cases of skin cancer and
about 9,800 skin cancer deaths in the United States.

Prevention efforts are focusing on kids, because sun exposure during
childhood can cause skin cancer in adulthood, according to Amy Malow,
director of sun safety for the American Cancer Society.

"A substantial amount of sun exposure occurs between the ages of zero
and 18; skin cancer does not happen because I got a burn last year,"
Malow said. "When you get exposed during your childhood, you're more
likely to develop it years later."

Adams Elementary in Livonia, Lathers Elementary in Garden City, O.L.
Smith Middle School in Dearborn, Northwood Elementary in Royal Oak and
Bailey Lake Elementary in Clarkston are among Metro Detroit schools who
received $500 grants.

While it's not a lot of money, sponsors hope it will raise skin cancer
awareness. They have used the money to publish newsletters and fliers,
hold special events and hand out sun safety items, such as sunscreen,
T-shirts and sunglasses, all with the goal of reducing kids' chances of
getting cancer when they grow up.

At Garfield, a meteorologist will visit this week to help kids do
science experiments that will demonstrate how strong the sun is. The PTA
also used part of its grant money for Frisbees that change color when
exposed to the sun.

Students at Northwood, in Royal Oak, had a sun safety poster contest.
Fifth-grader Emily Collick won the top prize, a $25 gift certificate.

"Every month in the newsletter we had a section on sun safety," said
Northwood PTA President Allison Sykes.

Dearborn's O.L. Smith Middle School also had a poster contest, with
hats, sunscreen, T-shirts, sunglasses and other sun safety items for the
winners.

"Just because they're out there for a few hours in the morning, it
doesn't mean (the sunscreen) is going to stay on all day," said Frances
Masalskis, whose son is in eighth grade at O.L. Smith.

"Lately, he'll put it on if he knows he's going to be out there," she
said of Austin Masalskis, 14. The American Cancer Society estimates
there will be nearly 2,000 new cases of melanoma reported in Michigan in
2005. Melanoma, the most serious form of skin cancer, is one of the
fastest-growing types of cancer in the United States.

Melanoma accounts for about 4 percent of skin cancer cases, but it
causes about 79 percent of skin cancer deaths.

Dermatologist Raechele Cochran Gathers of Eastside Dermatology in Grosse
Pointe Woods said everyone is vulnerable to the sun, regardless of their
complexion.

"Everyone needs skin protection, no matter what color they are," Cochran
Gathers said. "While it's true that African-Americans or people with
darker skin have lower risk, they certainly do get skin cancer.

"Even the darkest of skin can burn."

Cochran Gathers said parents can coax kids into using sunscreen by
buying Coppertone Water Babies glitter lotion in SPF 30. The company
also makes a green sunscreen spray that smells like kiwi fruit.

Neutrogena makes a sunscreen stick that kids can keep in their pocket,
Cochran Gathers added. Teens with acne should look for brands that say
"noncomedogenic" on the label, meaning it won't clog pores, she said.

Livonia mom Ginny Hall said her PTA will give clip-on bottles of
sunscreen to all of the kids at Garfield Elementary before their school
field day on June 7.

It's all part of the effort to teach kids how important it is to protect
themselves from the sun's harmful rays.

"Before we go out, we're going to go around to the classes and have
every child apply sunscreen," said Hall, who is the health and safety
coordinator for the Garfield PTA. "It's making them aware and making
them understand that it's dangerous to be out without sunscreen."
Comments (4805)

Skin cancer therapy being studied here offers hope Posted Thursday, May 26, 2005 by arjuna
May 26, 2005, 12:42AM


By TODD ACKERMAN
Copyright 2005 Houston Chronicle

Advanced skin cancer patient Jesse Newman was getting his final affairs in order last year when he began a Houston trial of an experimental new treatment.
graph

Newman had never heard of the approach — injecting an agent that triggers the immune system — but he figured it was worth a try. After all, his melanoma had withstood surgery and chemotherapy and spread to his lungs in tumors too numerous to count.

Seven months later, Newman is back to his old self, working in his shop, building things, playing golf. The therapy has killed 90 percent of the tumors in his lungs and is shrinking the rest. Doctors expect them to be gone soon.

"I'm a miracle melanoma patient," said Newman, 66, an Alabama resident who estimates he's traveled to Houston for treatment some 40 times since his diagnosis in 2002. "One day, I was preparing for the worst. Now, I'm living a normal life, enjoying every day."

Newman is one of a number of patients showing remarkable benefits from CP-675, one of the most promising therapies in development for advanced melanoma — as deadly as brain, lung and pancreatic cancers. Because it is particularly resistant to chemotherapy and radiation, current treatment options are extremely limited.

In midtrial results presented at a cancer conference last week, University of Texas M.D. Anderson Cancer Center researchers reported a 43 percent response rate from CP-675, a human antibody that works by a process known as immunotherapy. The treatment enlists the immune system to attack malignant tumor cells responsible for the disease.

Thirty patients with advanced melanoma got the injection. The cancers of five went into remission and eight more either shrank at least 50 percent or stopped growing.

The response rates for two FDA-approved therapies for metastatic melanoma — cancer that has spread to other organs — are significantly less. For one, DTIC, the rate is 6 percent. For the other, Interleukin-2, it's 10 percent to 15 percent.

Improvement cited
The M.D. Anderson trial also represented an improvement over the cancer center's previous trial with the injection, presented at the same cancer conference in 2004. Of the 39 patients in that trial, tumors disappeared in three, shrank in a fourth and stopped growing in five other patients.

That study involved single injections. The new study involves multiple injections.

"These new results are very promising for patients' metastatic melanoma, a population with a great need for new treatments," said Dr. Luis Camacho, an investigator in the study and an M.D. Anderson professor of melanoma medical oncology. "There are really no good agents to treat melanoma once it's spread."

Camacho estimated it will probably be two years before the drug's maker, Pfizer, can go to the FDA for approval of CP-675.

The antibody targets the receptor that works as "the brakes" of the immune system. Like a vaccine, it seems to continue working long after patients receive the injections. It may work well in melanoma, said Camacho, because previous research has shown that once activated, the immune system can recognize the cancer.

Cancer vaccines are another kind of immunotherapy, though they too harness the immune system to fight the disease, not prevent it. But they have been largely unsuccessful in melanoma.

Because the CP-675 antibody triggers the immune system to attack cells that "look" similar to the body's own, researchers worried that it might produce autoimmune disorders such as rheumatoid arthritis. But the only side effects observed — rashes, diarrhea and hypothyroidism — were easily resolved.

Newman said he had no side effects.

Melanoma is the cancer with the nation's fastest growing incident rate. Curable if caught early but deadly thereafter, it afflicts some 58,000 Americans a year, killing 10,000. Texas is one of four states with the highest incident rate.

Researchers are expected to start enrolling patients soon for a study comparing the antibody to DTIC. If successful, it likely would be the last study necessary for FDA approval.
Comments (9266)

Cancer scare became her cause Posted Wednesday, April 27, 2005 by arjuna
www.philly.com
Posted on Mon, Apr. 25, 2005
Body Language
By Art Carey
Inquirer Columnist

On that fateful day 16 years ago, Catherine Poole was five months' pregnant. She was lying on the couch, battling the flu, when she noticed something peculiar on the back of her right leg, just above the ankle.

She had always had a birthmark there, light brown and the size of a quarter. Now, it was raised and peppered with ugly black dots.

She knew a change like that was significant. The next day, she visited a dermatologist, who became visibly alarmed. A surgeon removed the growth immediately.

The pathology report: melanoma.

Poole had never heard the word before. She was shocked to discover she had a malignant form of skin cancer that, in its advanced stages, almost always kills, sometimes within months.

She worried whether the cancer would affect the child in her womb, whether she'd be alive to celebrate the baby's first birthday.

To eradicate cancerous cells in nearby tissue, a chunk of flesh the size of a golfball was cut out. A slice of skin was planed from her hip and grafted over the cavity in her leg. She spent the rest of her pregnancy on crutches, terrified the cancer would return.

"It was like sitting on a time bomb," she says. "I was told that if it's going to recur, it's likely to happen in the first two or three years."

Needless to say, the cancer didn't recur and Poole survived. From that experience came a friendship, a book, a vocation and a passion.

In those days, information about melanoma was scarce. Poole, a freelance writer and "congenital researcher," began digging. A mother lode was DuPont Guerry IV, director of the melanoma program at the University of Pennsylvania.

With him, she collaborated on a book that answered the questions Poole had when the cancer was diagnosed back in 1989, and then some. The second edition of Melanoma: Prevention, Detection, and Treatment (Yale University Press, $16.95) was just published. It is accessible, direct and practical.

When the first edition came out in 1998, Poole says, she began hearing from folks battling the disease. They were seeking further information, succor, guidance. She shared what she knew and offered a compassionate ear.

The demand for help inspired Poole to create the Melanoma International Foundation. She launched it in August 2003 with a credit card. It is based in her house in Glenmoore, Chester County. The staff numbers exactly one: Poole.

"I'm on call 24/7," she says. "If the phone rings, I pick it up."

The foundation's mission is education, prevention, early detection, and treatment research. It is supported by private contributions, many of which have come from grateful families and friends of melanoma victims aided by Poole in the last months of their lives.

Melanoma kills someone every hour, or about 7,800 people a year, often in the prime of life. (It's the most common cancer in women 25 to 29.) Our sun-worshiping ways, the popularity of tanning salons, and the Earth's thinning atmosphere (less ozone to block harmful UV rays) have helped boost melanoma rates. Its incidence is rising faster than any other cancer (2,000 percent since 1930).

How she developed melanoma is no mystery, says Poole, 52. A fair-skinned blonde, she spent her early years outside as a competitive swimmer in Arizona, where the sun is intense. One summer, when she was teaching horseback riding in Virginia, she was in the sun so much she actually tanned. In high school, she used a tanning lamp on her legs.

We are so enamored of a "healthy tan" (an unacknowledged oxymoron) that trying to dissuade us from spending time in the sun is futile, Poole believes. So recently, she has shifted her emphasis from prevention to early detection.

When out and about, she watches for telltale moles. And she isn't shy about urging people to consult a dermatologist pronto. She did it to a woman in her yoga class, to an airline clerk as she was about to fly out of town. When she sat behind George H.W. Bush at a conference, she noticed a lesion on his jaw. She encouraged him to have it checked. (He did; it was benign.)

The bad news about melanoma is that it's aggressive. The good news is that it's curable - if caught early. Poole's suggestion: With each change of season, examine your body for unusual moles and lesions.

She's no fan of sun-blocking lotions (most people apply too little, too late). Instead, she recommends staying in the shade and protecting your head and neck (where melanoma is especially lethal) with a full-brimmed hat, your body with solar-safe, tightly woven clothing. Her dream is to make using a parasol fashionable again.

"Your skin is not just a cosmetic shell," Poole says. "Your skin is an organ that protects all the other organs inside your body.

"Tanning is your skin's way of saying it's getting hit by radiation. The sun's damage is much deeper than mere sunburn. It's systemic; it affects the whole body. It's not only frying, aging and wrinkling your skin. It's bombarding your cells and messing with your immune system and DNA."

Comments (1926)

Melanoma Can Develop in Children Posted Wednesday, April 27, 2005 by arjuna
www.foxnews.com
Associated Press
Wednesday, April 27, 2005

CHICAGO — At age 10, freckle-faced Corey Halpin had bigger things to think about like basketball and Boy Scouts than the little black mole he noticed on his arm while camping.

At first, he thought it might be a tick. "I pushed it but it didn't move, but it bled," he recalled.

It wasn't until a few months later, during a spring 2002 visit to his pediatrician, that Corey casually asked his dad if he should mention the odd mole. That led to a referral to a specialist and alarming test results that caught even his doctors by surprise.

Melanoma (search), the most serious and potentially deadly form of skin cancer (search), was until recently almost unheard of in children, and it was a diagnosis that his family wasn't prepared for.

"My husband and I were scared to death" and so was Corey, said his mother, Marge Halpin.

Pediatric melanoma (search) is still uncommon in children, affecting only 7 per million, or about 500, according to 2002 statistics from the National Cancer Institute. But that number has risen from 3 per million in 1982.

Dr. Charles Balch of the American Society of Clinical Oncology, who has specialized in melanoma for 30 years, saw his first pediatric case five years ago. Since then, Johns Hopkins Hospital, where he works, has treated about 20 youngsters, the youngest just 8 years old.

Dr. Anthony Mancini, dermatology chief at Children's Memorial Hospital in Chicago, diagnosed Corey Halpin's melanoma and said he and his colleagues have treated eight cases in the past nine years, about double the number seen in the previous two decades.

Recent studies also report increases in England, Sweden and Australia.

"There's an appropriate level of alarm here," Mancini said. "Clearly it's happening and it's deadly, and it's missed."

Some pediatricians who see unusual moles in children "would ordinarily dismiss this as nothing because melanoma is not supposed to happen in this age group," Balch said. "We all should be aware that this can occur and biopsy suspicious or changing moles in children."

Balch said reasons for the increase are uncertain. Some doctors think it might be from depletion of the ozone layer, which protects the Earth from some of the sun's damaging ultraviolet radiation. Others attribute it to excessive sun exposure and blistering sunburns in early childhood, though some experts had thought it took much longer for skin damage from repeated sun exposure to develop into cancer.

Melanoma prevalence has risen in adults, too — more than doubling in the past 30 years, according to the cancer institute. The American Cancer Society estimates that this year about 60,000 U.S. adults will be diagnosed with melanoma and that 7,700 will die from it.

Melanoma develops in skin cells called melanocytes, which produce the pigment that colors the skin's surface and protects deeper layers from sun damage. It is much more invasive and likely to spread to other parts of the body than other skin cancers

Research from Italian doctors published in the March edition of Pediatrics found that melanoma lesions in children sometimes look different from those in adults and may be misdiagnosed.

In adults, melanoma often looks like a black or very dark brown mole, or one with irregular borders. But half the Italian children studied had lighter-colored lesions, and most had well-defined borders.

Also unlike adults, most children with melanoma have no family history of the disease, and they may lack other risk factors including moles present since birth, Balch said.

Corey Halpin, of Hanover Park, a Chicago suburb, has no relatives with melanoma or any other kind of cancer. But he does have other risk factors — fair skin, red hair and green eyes.

Mancini, his doctor, says the traditional A-B-C-D signs of melanoma — asymmetry, border irregularities, colors of mixed black and brown, and diameters larger than a pencil eraser — sometimes occur in children. But a child's lesion also can be smaller and pinkish. Mancini recommends the "ugly duckling" detection method — watching for a mole that looks completely different from the child's other moles.

In Corey's case, the mole was tiny but much darker than his other freckles, and it bled — another warning sign.

Corey has always been sensitive to the sun, though his parents say they're much more vigilant about using sunscreen since his diagnosis.

Three years since his surgery, Corey is cancer-free. He still has tests every few months, but doctors say his long-term survival chances are excellent.

The angry scar on his arm has shrunk as he's grown but it will always be a reminder. His pediatrician told him that it would be like a battle scar he could use to impress girls.

Now 13, Corey smiles at that thought. Comments (16876)

Stay sun-smart Posted Friday, April 8, 2005 by arjuna
Apr 4 2005

By Craig Thomson, The Evening Chronicle

A Newcastle University professor has revealed children are three times more likely than their grandparents to get skin cancer. Craig Thomson reports.

**********

As the weather warms up and thoughts turn to summer, many people are planning their holidays.


But research has revealed that many of us could be putting our lives at risk as we soak up the sun this year.

Prof Brian Diffey of Newcastle University says new figures show rates of melanoma are rising sharply in younger people and the statistics are set to double in the next 30 years.

More than 7,300 cases of malignant melanoma are diagnosed in the country every year, with 1,700 people dying from the disease.

Prof Diffey's work has shown that melanoma is now attacking younger people more often as each decade passes.

The sun protection specialist, who is now heading the SunSmart campaign to reduce the mortality rates, said: "Acting promptly can save lives and early detection and treatment will give many melanoma patients an excellent prognosis."

Signs to watch out for include a mole getting bigger, a mole with a ragged outline or one with a mixture of different colours.

If a mole gets inflamed or starts to bleed or itch, then people are advised always to go to their doctor and get it checked out.

More than 7,000 people a year in the UK are diagnosed with malignant melanoma.

It usually develops in cells in the outer layer of the skin but can spread to other parts of the body.

It is the second most common cause of cancer among young people aged 15 to 34 and early detection is crucial for successful treatment.

Latest research suggests sunburn in childhood can double the risk of melanoma in later life.

Dr Mark Birch-Machin, another skin cancer specialist from Newcastle University, says he would support guidelines to restrict young people's access to sun beds.

He said: "You get between 50% and 80% of your total lifetime's sun exposure before you are 21 years old.

"These young people who expose themselves to so much sun don't realise they are damaging their DNA and significantly increasing their chances of getting skin cancer."

This year's SunSmart campaign aims to target young people between the ages of 16 and 24, issuing warnings than sunburn can more than double their risk of skin cancer.

An web game has even been designed to highlight the important message.

All schools across the North East will be offered free posters, lesson plans and activity sheets based on SunSmart messages, while all health professionals in the region will be sent posters giving a guide to suspect moles and lesions - along with posters to help patients become sun-smart.

Prof Robert Souhami, executive director of policy and communications at Cancer Research UK, said: "It is important to persuade people, especially youngsters and those with fair skin, to avoid excess sun exposure and burning.

"We know that half of all cases of cancer can be prevented by making lifestyle changes.

"We are seeing more and more people giving up smoking to lessen their chances of getting a whole range of cancers.

"Reducing the risk of cancer is something most of us can do by following the SunSmart code."

Page 2: I will never go on a sun bed again

I will never go on a sun bed again

Emma Foggon knows better than most the dangers caused by too much exposure to the sun's harmful rays.

In the past 12 months, she has gone under the surgeon's knife twice after being diagnosed with skin cancer.

Emma, 29, from Wardley, Gateshead, said: "Being diagnosed was a total shock, I just couldn't believe it.

"I've got dark hair, dark eyes and I tan easily, so I thought I wouldn't be at risk."

Emma, an administrator at St Oswald's Hospice in Gosforth, was diagnosed by her GP after she got him to check out a patch of coloured skin on the back of her thigh.

After results from a biopsy proved she had the disease, surgeons at North Durham University Hospital removed the skin patch in November last year.

Emma added: "I used to be a sun worshipper and use sun beds, but after my experience of skin cancer I will never go on a sun bed again.

"I think it is really important to highlight the dangers of skin cancer - and it is very important to be vigilant.

"If you think there is a problem, get it checked out."

********

Look after your skin

The SunSmart code recommends you:

* Stay in the shade between 11am and 3pm;

* Make sure you never burn;

* Always cover up with a T-shirt, wide-brimmed hat and sunglasses;

* Remember to take extra care with children;

* Use factor 15-plus sunscreen;

* Report any mole changes or unusual skin growths promptly to your GP.

Page 3: Pioneering therapy

Pioneering therapy

A team of North East scientists has pioneered technology that could open the doors to many revolutionary cancer treatments.

Staff at BioTransformations Ltd, a spin-off from Newcastle University, has developed a process called light-activated therapeutics.

The process involves taking cancer-targeting antibodies and cloaking them in a compound sensitive to light, rendering them harmless for entry into the body. The antibodies attach themselves to the cancerous growth and, when exposed to light, are activated to either directly kill the tumour or carry toxins to destroy the cancerous tissue.

The Centre of Excellence for Life Sciences, the Government-funded body charged with nurturing the region's healthcare and life science economy, has provided funding and support to BioTransformations in preparing the technology for clinical trials.

Janette Thomas, centre project director, said: "This is the first development in the world to use light to direct the body's own immune response to a specific area."

The process could enter clinical trials within the next 12 to 18 months.


Comments (1213)

Basking in ignorance Posted Friday, April 8, 2005 by arjuna
www.timesonline.co.uk

March 23, 2005

Reckless exposure to the sun has led to a surge in skin cancer

More than 7,300 cases of malignant melanoma, the most virulent form of skin cancer, are diagnosed in Britain each year, and more than 1,700 people die from the disease. This form of skin cancer, if not treated in time, is one of the most deadly. It is also one of the most avoidable. Figures published yesterday, however, suggest that the incidence of melanoma is rising fast. It will treble over the next 30 years, making it one of the five most common cancers. Todays children are three times more likely to contract malignant melanoma than their grandparents. The reason is almost wholly attributable to ignorance. Thousands of lives can be saved; but only if Britons understand what causes the disease and what they must do to avoid it.

Skin cancer is, overwhelmingly, caused by strong sun. For centuries, pale-skinned Northern Europeans faced no danger. The summer sun was intermittent and relatively weak. Those labouring in the fields wore garments that covered most of their bodies. Those with wealth and position considered fair skin a mark of gentility, and took care not to expose themselves. But fashions, as well as lifestyles, have changed. For three generations a suntan has been essential to any model or film star, has been the boast of those able to afford foreign holidays and has been the single-minded goal of young people spending hours prone on the poolside sunbed.

Only now is the cost of this obsession becoming apparent. Skin damaged early in life by sunburn or prolonged exposure is much more likely to develop cancer. Often this is harmless. But malignant melanomas are nowadays attacking the young as well as the old. If their cancerous cells are not to spread, the disease must be diagnosed early and treated rapidly.

Diagnosis should be simple but is not. Moles that become larger or patches of skin that turn dark, rough or inflamed should be investigated. They are easily removed, and doctors are well aware of the dangers of delay. The problem is that patients either do not notice or do not realise the urgency. Medical research is only beginning to catch up with the scale of this issue.

What is urgently needed is a sustained campaign to make more people aware of all the dangers. A survey in 2003 by the Office for National Statistics found that although 75 per cent of people questioned knew that sun could cause cancer, only 6 per cent kept out of the midday sun. Indeed, most tourists regard sunbathing as essential to any holiday and 70 per cent believe a suntan will make them look healthier or more attractive. More culpably, only 0.3 per cent said they would have suspect moles checked.
Emigration and tourism have made this problem far more urgent. The influx of fair-skinned people into Australia and California led to sharp rises in melanoma, and only now, after a 20-year campaign, are Australians beginning to understand the dangers and changing their behaviour. Britain is no sun-soaked paradise. But Britons, too, must change, especially on holiday. Otherwise they could pay for their sun worship with their lives.

In the eye of the beholder Posted Friday, April 8, 2005 by arjuna
Although little is known about eye cancer, some advances are making patients' lives easier

Robin Summerfield
Calgary Herald

Thursday, March 17, 2005


Sarah couldn't focus. Contact lenses didn't help fix the blurriness and her peripheral vision began to go.

Then, during an Easter lunch date with a friend one year ago, her sight failed.

"Half the menu was black," says Sarah, who nonetheless didn't panic that Friday afternoon. "I just felt there was something that wasn't right, but I just didn't know what it was."

The mother of two went directly from lunch to her optometrist. Monday morning, she was at a specialist's office. (At Sarah's request, her name has been changed for this story.)

The specialist found a large mass, about 12 to 15 millimetres deep, in the Calgarian's right eye.

"I was shocked. It was like it was happening to someone else, not me," she says.

"It was life-threatening. I remember he used those words, life-threatening."

The 47-year-old had eye cancer -- an extremely rare form that effects only six people per million per year in Canada.

In Alberta, about 15 to 20 cases are seen each year.

In Sarah's case, the diagnosis was choroidal melanoma -- a form of eye cancer that attacks blood vessels beneath the retina.

But melanomas -- those cancers most commonly associated with sun exposure on the skin -- can occur in various eye sites.

Uveal melanomas can grow on the eyelid, the iris, the film over the eyeball, the choroid (as in Sarah's case) or in the orbit, which is the fatty tissue between the globe and the skull.

Other cancers, including retinoblastoma, epidermid cancers and adenocarcinomas, are also found in the eye.

They start as freckles or spots on the eye and are usually detected during routine eye exams. Freckles on the eye are quite common with one in 100 people developing a spot.

Most remain benign; a few grow cancerous cells. The rarity of eye cancer has left scientists, physicians and researchers with many unanswered questions, despite much investigation.

"We've got a long ways to go. Our overall cure rate hasn't improved over the last 25 years," says Calgary ophthalmologist Dr. John McWhae, considered the city's top eye cancer specialist.

Physicians can save vision "more often than 20 years ago," but we haven't moved forward in curing or preventing eye cancer from spreading, McWhae says.

Alberta's perpetual sunshine means more people here are likely getting eye cancer compared to other places but, "it's hard to prove because the statistics are not there," McWhae says.

Here's what is known: Eye cancer has no known cause or genetic marker; it is more prevalent in blue-eyed, fair-skinned people and in Australians; and if it spreads, an estimated 85 to 99 per cent of the time it will spread via the blood to the liver, where the eye cancer cells find the only hospitable environment in the body in which to grow.

Treatment can range from chemotherapy to radiation to removal of the eye, the lids and other tissue in the area.

Advances are slowly being made in treatment and reconstruction post-eye removal, but there are still many unanswered questions about cause and cure.

Statistics would help to move eye cancer research and understanding forward, but its rarity precludes that, says Dr. Steve Rasmussen, a Calgary-based surgical pathologist with Calgary Laboratory Services.

The epidemiological statistics an expert would need to make confident conclusions about cause are not available, says Rasmussen, who estimates he biopsies about one cancerous eye per month.

"We are just scratching the surface, because there is so much we don't know about cancer," says Rasmussen, also a clinical associate professor at the University of Calgary.

Surgeons removed Sarah's right eye on June 3, 2004, just one month after her fateful Easter lunch.

"It's really hard to explain when you first look at yourself and you have no eye," says Sarah, who works as a business and industry instructor. "It's shocking and devastating, but you also realize you have to move on, too."

She stayed in hospital for three days and recuperated at home for two days.

"I said to myself, 'I'm just going to move on from here,' " says the 48-year-old. "I realized I had to show strength for my kids. I had to say to them and show them, 'Mom's fine.' "

"Fewer and fewer people are having to have their eyes removed because the treatments are becoming much more advanced," says Dr. Paul Finger, an eye cancer specialist at the New York Eye Cancer Center in New York City.

Tumours are divided into three sizes and treated accordingly. A mass of three millimetres or less is considered small and can be treated with radiation. A mass of three to 10 millimetres is considered medium sized and can be treated with radiation or surgery. However, a mass larger than 10 millimetres means the eye must be removed.

Eye plaque radiation therapy, the implantation of a disc impregnated with low level radiation that targets the tumour during radiation treatment, while simultaneously shielding the healthy eye, is one procedure. Chemotherapy can also be administered orally, intravenously or topically as eye drops. (However, using chemotherapy is not often used to treat eye cancer, says McWhae.)

"Very few tumours have to be removed these days because we are finding them smaller and smaller," says Finger.

So what can people do to protect themselves? Physicians agree sunglasses can't hurt and regular eye exams will help catch the disease sooner.

Sarah took off the bandages within days and lived in sunglasses until she was fitted with a prosthetic eye in Vancouver on July 20, 2005, just six weeks after her surgery.

Doctors stitched a coral implant -- a piece of coral wrapped in sclera (the white of the eye) from the eye bank -- into her eye cavity and connected the muscles. Her new eye is a custom-made, removable half globe that sits snugly inside the coral implant with the help of suction.

The eye, a striking green hazel, perfectly matches the colour of her left eye. Unless Sarah pops it out, which she does once a month to clean it, one would be hard pressed to know it's not real. The only hint the eye isn't normal: it stays fixed, looking straight ahead, but that could be explained away as a lazy eye.

Her top and bottom lids close naturally around her artificial eye, completing the illusion.

She is looking to have another surgery that would permanently screw the half globe into the coral implant and create "extreme movement," she says. If successful, both eyes would move in sync.

Calgarian Roxana Anderson's eyes will likely never move in sync, despite advances in science.

Twenty years ago, she lost her right eye, the lid and much of the surrounding tissue with meibomian cell carcinoma, a cancer that attacked her eye lid. She was left with a 11/2 -inch wide gaping hole in her face.

"It was socially isolating and emotionally devastating," says Anderson, who later joined About Face, an international support group for people with facial differences.

Her first prosthetic was held in place with contact cement, it often jutted out a half inch from her face, took 40 minutes to get in place and she constantly worried it would pop out. So she avoided going out.

"It wasn't worth the effort," says Anderson, now 56.

In 1991, she found a more natural answer at the Craniofacial Osseointegration & Maxillofacial Prosthetic Rehabilitation Unit inside Edmonton's Misericordia Community Hospital.

Using surgery, implants, facial and oral prosthetics, surgeons and specialists rebuild and repair patients with head and neck defects caused by cancer, infections, trauma or birth defects.

They build ears, eyes, brows, noses, jaws and cheeks.

The goal is perfect-looking, or as near to natural-looking, prosthetics as possible.

"If someone had it and you walked by them on the street, unless you stopped and looked, you be hard pressed to know," says prosthodontist Dr. Johan Wolfaardt, the unit's executive director.

In Anderson's case, titanium posts implanted in bone anchor the implant to her face.

Doctors have built her an eye, a bit of cheek and brow using silicon. Her implant includes freckles, wrinkles and extra hair at her brow that match her existing eyebrow.

"There's a lot of artistic work that goes into these prosthetics," she says.

Physicians and researchers have more than artistry in mind when it comes to vision.

"In the long term, and this may sound like science fiction, we will be looking to restore vision," says Wolfaardt, from Banff, where he attended an international conference of specialists in the field.

Next month, Sarah completes her masters in education in adult and higher learning at the U of C. She is thinking about going for her doctorate. She is an avid reader, still drives and loves to downhill ski.

"I just felt that I wasn't going to let it change my life, take over my life, or defeat me."

Cancer, says Sarah pointedly, "doesn't have to end your life."

rsummerfield@theherald.canwest.com
© The Calgary Herald 2005 Comments (179)

Melanoma in Children Appears Different Than Adult Disease Posted Friday, March 11, 2005 by arjuna
Survival rate in young kids is higher, small study finds

By Janice Billingsley HealthDay Reporter

FRIDAY, March 11 (HealthDay News) -- A small study of 33 Italian children with melanoma found those children who were under 10 at the time of diagnosis had higher survival rates than those who were older when they were diagnosed.

The researchers also found the disease sometimes appears differently in children compared to adults.

"Our findings give the impression that melanoma behaves differently in the younger age group," report the researchers, from the Pediatric Oncology Unit at the Istituto Nazionale per lo Studio e la Cura dei Turmori in Milan.

Other health experts acknowledge that some of the findings are interesting, but caution against jumping to conclusions on the strength of such a small study.

"There are some patterns of note -- it does raise the possibility that there may be something different biologically in the melanomas of children -- but the study is very small, and there is very little one can say," said Kathleen Egan, an associate professor of medicine at Vanderbilt University School of Medicine in Nashville.

The study appears in the March issue of Pediatrics.

For the study, the researchers analyzed data on the 33 children, who had been diagnosed with the skin cancer before the age of 14. Melanoma is the rarest, but most deadly, of the three skin cancers, with about 54,000 new cases diagnosed each year in the United States, according to the National Cancer Institute. While the prevalence of melanoma is increasing -- rates have doubled over the last 30 years -- it's still rare in children.

The severity of the disease among the 33 children ranged from cancerous skin lesions, to cancer that had spread beyond the initial tumor. Most of the lesions were found on the legs. Surgery to remove the cancer was the primary treatment.

With a median follow-up of 11 years, 60 percent of the children experienced five-year-event-free survival, and overall survival was 70 percent. Divided by age, however, those under 10 years at the time of diagnosis experienced a 90 percent, event-free survival rate compared to a 47 percent event-free survival rate for those who were older when they were diagnosed.

This was true even though the initial cancer diagnosis seemed worse in the younger children as measured by the thickness of their lesions. The researchers suggest that the reason younger children had more serious cancer initially is because the disease is so rare in young children that doctors might not look for it.

Also of note, the researchers said, was that the lesions found in the children were somewhat different than those typically found in adults. There were more amelanotic lesions, which are lesions that lack melanin -- the natural substance that gives color to hair, skin and the iris of the eye -- and the lesions were generally thicker than those in adults. Also, most of the lesions were found on the children's legs, which is not the case with adult melanoma, the researchers said.

"It is generally assumed that childhood melanoma behaves biologically like its adult counterpart, but our results make us wonder whether this is really so," the researchers wrote.

Egan said that, due to the small number of children in the study, there's a risk the findings might be unique to that group of kids, and may not apply to children in general. But, she added, it would be hard to find a larger group because the disease is so rare in children.

The findings are useful because they can alert parents to the fact that children can get melanoma, and it's often diagnosed, Egan said.
"The last thing anyone wants to think about is looking at cancer in an 8-year-old, and there is also a natural abhorrence to doing a biopsy on a small child," Egan said. So if parents are concerned, they should take their child to a dermatologist who specializes in melanoma and can spot any suspicious lesions early, she said. Comments (35)

Hillhouse to shine light on skin cancer with research Posted Saturday, March 5, 2005 by arjuna
East Tennessean - LifeStyle

Issue: 3/3/05 By David Bryant

Skin cancer is the fastest growing cancer in the world. It also happens to be the most expensive cancer to treat, with different types surfacing rapidly. Melanoma alone kills about 8,000 people a year, the American Cancer Society says. That's the "big picture." ETSU Health Psychology Professor Dr. Joel Hillhouse has chosen to focus his cancer research on a sample of the public he interacts with every day - students. Hillhouse has received a $1.3 million ACS grant to help aid in his research to prove tanning beds cause skin cancer. His research will specifically study the effects of tanning on the skin's appearance, he said. "Most college students know the health risks involved and choose to ignore them," Hillhouse said. "Hopefully with showing how tanning hurts their physical appearance we can reach them better." In a pilot study performed in 2000, Hillhouse used about 40 students to probe the effects of tanning on the skin. By showing the students that tanning caused their skin to thicken, age and wrinkle, Hillhouse was able to reduce their tanning visits by as much as 50 percent, he said. The ACS could not ignore Hillhouse's results, he said. College students are Hillhouse's key focus because studies have shown that the highest frequency of tanning happens between ages 18-25. Scott Hammerbacher, a 21-year-old student worker in ETSU's Psychology Department, admits that after hearing Hillhouse's argument he has significantly reduced his visits to the tanning bed. "I think that this is a unique way of educating college students on some of our unhealthy habits," Hammerbacher said. "I feel that tanning bed shops really do not express the possible side effects associated with tanning and that's misleading." One of the biggest misconceptions people have about tanning is that it is healthy for you, Hillhouse said. That simply is not possible, he said. So, is Hillhouse trying to put a lid on the $4 billion industry? "My job is not to shut down tanning beds immediately," he said. "It is to educate young people on how tanning beds can hurt them." A slow transition of turning tanning beds into skin care facilities over time, however, is one of his goals, Hillhouse said. First, though, money from the grant is being used to set up the laboratory for the study. ETSU provided an unfurnished lab and Hillhouse is acquiring all the necessary equipment. Then Hillhouse will hire a coordinator and research assistants. Finally toward the end of this summer, he will begin to randomly select the students to participate in the study, he said. In addition to his 10 years in skin cancer prevention work, Hillhouse has the passion for health psychology - and a certain amount of timing and what he calls luck. "Some of it is serendipity," he said, "but I genuinely have an interest." Comments (13)

Don't ignore nails Around Kentucky Posted Tuesday, February 1, 2005 by arjuna
Wednesday, January 26, 2005


By Byron Crawford The Courier-Journal

While removing nail polish nearly a year ago, Lynda Sherrard of Frankfort noticed a dark streak halfway down the middle of her right thumbnail.

"It looked like somebody had run a fine-tipped pen down the nail from about midway to the end," she said. "I thought it looked odd, but I didn't know what it was."

Sherrard, 60, mentioned it to her family doctor, who thought it might have been caused by a splinter and saw no need to be worried. Another doctor guessed it was a symptom of aging.

About six months later, Sherrard said, The Courier-Journal ran an article about what your nails tell you about your health.

"This thing had never grown out, so I read through the article, and one of the things it said was that if you have a vertical black streak in your nail, see your doctor immediately. That was when I began to worry," she said.

Biopsy done

Eight months after Sherrard discovered the dark line, doctors at Lexington's Dermatology Associates of Kentucky took a biopsy of both the nail and the thumb and discovered she had a form of skin cancer known as keratoacanthoma, a low-grade malignancy that was surgically removed.

"The doctor did indicate that it was one that spreads," Sherrard said. "He made the comment that he was glad I came when I did, and he said that I had been in danger of losing at least a digit of my thumb."

Dr. W. Patrick Davey of Dermatology Associates notes that streaking of nails occurs naturally in a large percentage of dark-skinned people and is rarely a cause for concern among that group. Among fair-skinned individuals, however, dark streaks on the nails, especially under a single nail, generally raise suspicion among doctors and should not be ignored.

It may be a mole, or . . .

"Most commonly it ends up being a freckle or a regular old mole that's causing the problem with the streaking," Davey said. "I've been doing surgery on the nails since 1988 and have yet to really find a melanoma. But I think the message is that if you have this kind of change in your nail, it could be a skin cancer."

Davey averages a surgery about every two weeks on patients who have developed some form of skin cancer under fingernails or toenails.

"When you reach a certain age you see a lot of bumps and discolorations on your skin that you tend to take for granted," said Sherrard, an antiques dealer in Versailles.

"I've had a friend that, since this happened, said, 'You've got me studying my nails every day.'
"She came in one day over at the antique mall and said, 'You won't believe this, but a friend of ours just found a melanoma under her toenail. We'd never heard of any of this until you started having the problem with your thumb.' " Comments (27)

An online chronicle of grief Posted Tuesday, February 1, 2005 by arjuna
A young widow pours her sorrows into an online journal, opening a window onto modern mourning

Tuesday, February 01, 2005 By Alana Semuels, Pittsburgh Post-Gazette

Online journal entry by Rich Rust, before his death:

"I think I've probably mentioned several times, if not several hundred times that I have been sick recently. Flu-type stuff. But in addition there have been strange aches and pains, unexplained back and neck aches. I've basically felt like crap for about a month or so.

My doctor thinks I'm nuts. I can see that in his eyes. I had this bizarre chest pain a few weeks ago, that was probably from Madison kicking me. But it was REALLY painful, so I decided he should know about it. Yeah, he didn't think much of it. Ran some tests, yadda yadda yadda, I'm fine."

A life online

Friends and family of Pittsburgh musician Rich Rust could follow his life online. They heard about the antics of his 2-year-old daughter, Madison, about practice sessions with the popular Pittsburgh band Breakup Society, and about the melanoma that was taking over his body although doctors didn't know it at the time.

Even now, anyone can read about how the 32-year old Rust felt sick for weeks, went to his doctor and was told he had a urinary tract infection and got the anti-anthrax drug Cipro. They can read about how he felt so sick he could barely function, how his mother told him he looked green, and how he finally went to the emergency room, where he was told the deadly skin cancer had returned.

His last entry, posted on Dec. 24, 2003, reads, "went to ER and my melanoma has come back. It's now in my liver and my spleen. Merry Christmas! I'll post all the gory details in the journal as soon as I get a chance."

He died Jan. 11, 2004.

Rich's death plunged his wife into the deepest sorrow imaginable. Deni Rust slept for the months after he died, and woke up early one May morning and took herself to the hospital to give birth to the couple's son, Ethan.

But even after her second child's birth, Deni Rust could not go more than a few minutes without breaking down and crying or missing her husband of three years and partner of almost eleven. She had panic attacks, thoughts of suicide and even checked herself into UPMC Western Psychiatric Hospital and Clinic for a night at the urging of her siblings and friends.

Deni Rust, 34, of McCandless, continued her husband's journal after his death, using the Web site he created to immortalize his writings, to establish a guest book where friends and family can share memories, and to post her thoughts as each day passes.

A year later, Deni Rust still struggles to live with her grief. Her Web journal has become part catharsis, part weekly update, part cry for help. She has received e-mails from faraway strangers who offer support, and she believes the journal is, in a way, necessary for her to survive.

Rust's journal is a touching and terrifying window into the age-old process of grieving, but it also is on the forefront of a new trend: online journals in which writers share their illness or personal tragedy, where readers can follow along, sharing every moment, no matter how personal, with complete strangers.

Journal entry by Deni Rust, March 15, 2004, after her release from Western Psych:

"Now, let's remember what helps me to feel better: talking about my feelings! This is a release for me. This is why I keep the journal. I don't have my husband to talk to anymore. I need to rid myself of anger and pain and this is how I choose to do it. It works for me. It comforts me to receive e-mails from people who tell me they read the journals and care about Rich and our family. I need this to get through every day."

Catharsis

Type in "health blog" into the search engine Google and you'll see journals describing people's journeys through anorexia or dealing with HIV, many of which were created in the past year. Philadelphia Inquirer reporter Fawn Vrazio legitimized the genre when she started her "cancer chronicles blog" in November 2004 as part of the newspaper's Web site. She urged her readers to "think of it as a journey into a world that many fear but few understand."

Reading some of these blogs is like rubbernecking at the scene of a car accident -- it's difficult to watch but impossible to turn away.

But with their rising popularity, these journals may become the next big thing, said Amanda Lenhart, a research associate at the Pew Internet & American Life Project. During the recent presidential campaign season, political blogs were widely read as insider scoops. Online journals may serve both as ways for those going through a health crisis to talk about it and to promote awareness about various illnesses and conditions.

Blogging itself -- or posting a journal or opinions online -- is becoming more mainstream: Blog readership went up 58 percent in 2004, according to a Pew survey. More than a quarter of Internet users read blogs, and more than half of blogs are in a diary style.

"People tend to be a bit more confessional on the Internet," Lenhart said, because it's easier to share thoughts with people who are not right in front of you or on the phone with you.

This applies especially to sensitive topics. "There might be times when you want it to be a one-way exchange," Lenhart said. "It's hard to hear people respond to your grief, and in some ways it's easier to talk about things online."

This catharsis is one of the reasons Deni Rust turned to a Web journal. But there were other reasons: she wanted to remember the last few weeks of her husband's life, she was furious with the doctor who seemingly missed the cancer's recurrence. She hated hearing the well-meaning consolations of people who didn't know what to say.

And after weeks and months of these feelings, she wondered if those who were asking about her well-being perhaps were not as concerned as they had been in the raw days after Rich Rust's death.

But most of all, she needed to get her rage, anger and sadness out. "It definitely is therapeutic," Rust said in an interview at her home. "Usually I write when I'm at my darkest moments, and by writing it down and getting it out, it helps."

Keeping a journal is just one therapy recommended for grieving people. Although every person mourns differently, journaling allows people to see how they are progressing, said Jean Haller, who teaches journal workshops and owns the Journey of Life bookstore in Shadyside.

Private journals are more common, Haller says, but she has seen students benefit from journaling or blogging in an online community or Web site. "Writing is a great catharsis for any problem, but especially with grief."

Journal entry by Deni Rust, Jan. 10, 2005, on the eve of the one-year anniversary of her husband's death:

"I'm so afraid and sad and no one can help me. I decided not to seek out any professional therapists because they can't tell me anything I haven't thought on my own or could read in a book. Besides, it's not my mind that is damaged, it's my soul."

Support

Since her husband's death, Deni Rust has had difficulty finding support. With two children to raise, she keeps herself busy, but still depends on a close-knit group of family and friends to cover for her in times of crisis.

Her best friend, Kim, cut Ethan's umbilical cord when he was born, and Rust's parents and friends babysit the kids on the rare occasion that Deni Rust ventures out into the world.

She tried going to a widows support group, but was the youngest person there by a decade. She went to a counseling session recommended by a therapist, but the other participants were there because they had anger management issues or were ordered to the session because of domestic violence; this didn't seem close enough to Rust's own situation.

"I feel alone in my grief," Rust said, "but I know it can't be so."

Young people tend to avoid support groups in general, said Lulu Orr, the executive director of the Good Grief Center for Bereavement in Homestead.

And with no other means of support, it's often difficult for them to find a way to talk about what they're going through. "People can get really tired of hearing about it," she said. "But people that are grieving need to tell their story over and over. The more they talk about it, the more believable it becomes to them."

Thus far, writing works best for Deni Rust. She receives e-mails from people from around the world sharing their own stories of loss or offering advice on how to cope. She is not alone in finding these journals beneficial; one of the country's most popular journaling sites, LiveJournal.com, includes other journals like Deni's.

It helps to share your feelings with people who understand what you're going through, said Carol Young, a widow who helped create YoungWidow.com, an online support group, after the terrorist attacks of Sept. 11, 2001.

"You're feeling all these emotions, and nobody seems to understand you," Young said. "Unless you've been there, you really can't understand."

Journal entry by Deni Rust, May 4, 2004, right before Ethan's birth:

"It is sickening and horrifying how a mole -- a mole -- stole his life. ... Cancer is ugly and devastating in no matter what form it attacks. My friend Kelly's sister April told me the other day that Rich is her hero. She and a friend decided to make an appointment to have their moles checked ... They found acute lymphatic leukemia ... She never would have gone to the doctor if it wasn't for [Rich].

Awareness

It's hard not to read Rich Rust's blog and worry about that mole on your shoulder or that day you went outside without sunscreen. His progress from a happy and busy father to a patient whose illness was overlooked would make even the most hardy reader feel weak.

Rust, who played in many Pittsburgh bands as keyboardist and singer, was diagnosed with melanoma in May 2001. He had two surgeries in California, where he and Deni were then living, to get rid of the cancer, and was seeing an oncologist every few months in Pittsburgh after they moved back here. After the surgeries and new therapies, he hoped he had the cancer beat.

Deni Rust says she still receives e-mails from friends who decided to get a mole checked out after reading his story.

Family and friends have taken care to make sure that neither Rust's sunny personality nor his difficult story are forgotten; already two benefit concerts have been held in his memory, and at the first concert a friend of Rust's released a CD, "The Rich Rust Experience" featuring songs Rust wrote and sang. His wife tentatively talks about holding these concerts annually, and donating the proceeds to a melanoma awareness society.

But Deni Rust's journal is educational as well, as a window into the mind of a grieving widow. She says that the knowledge that others are reading and understanding how tough life can be is one of the things that keeps her writing.

"I have to talk about it -- it's a relief to talk about it," she said in an interview. "I have to let people know that things could be worse ... we all have tragedy in our lives."

Journal entry by Deni Rust, July 12, 2004, on her wedding anniversary:

"Madi always pretends to call her daddy. Usually it is when I pick her up from school and her class is playing outside and we have to walk through the 4-year-old room to leave. She will stop and pick up the toy phones and pretend to call him on each one. I patiently wait for her and try my hardest not to cry. ... In the car the other day she "called" daddy and said, "Hi daddy. Watch you doin'? I want to come to heaven with you, daddy. No, no no, I want to come to heaven with you, daddy." I almost had to pull the car over. Once again my heart broke. I found it so strange that she said, "... no, no, no... " It was almost if he told her she had to stay here with me -- that I need her."

The online journals
You can read Deni Rust's journal at www.richrust.com. Comments (29)

Antarctica May Hold Cancer Key Posted Tuesday, February 1, 2005 by arjuna
Published: Feb 1, 2005


By KURT LOFT

TAMPA - A University of South Florida scientist may have won another battle in the war on cancer.

Organic chemist Bill Baker has isolated a compound in an exotic marine creature that shows promise in treating melanoma, the most deadly form of skin cancer.

``This is the sort of thing we chemists wait for,'' Baker said Monday.

Along with fellow scientists from the University of Alabama, Baker has been working in Antarctica, where animals have evolved to survive in the extreme environment.

One such critter, a spongelike tunicate, is thought to be a rich source of compounds that might help people fend off disease.

Baker's team extracted a defensive toxin that disrupts the physiological pathways in predators. Although the toxin is bad news to anything wanting to munch on the tunicate, also called a sea squirt, the compound acts chemotherapeutic in the laboratory.

Scientists at the National Cancer Institute in Maryland tested the material against more than 60 kinds of cancer cells. The compound, called Palmerolide A, had little effect on all but one: It zeroed in on melanoma cells and killed them.

``What you look for is a pattern,'' Baker said. ``If you have a cytotoxin that kills a lot of different cancer cells, that's not what you want. What you do want is only a few cell lines that show sensitivity to the compound.''

Baker got it.

``Melanoma not only was selective, but the compound was potent,'' he said. ``That's what's really neat.''

Baker and his colleagues have made eight trips to Antarctica to study animals and plants for possible pharmaceuticals. About 60 percent of marketed drugs come from natural sources. The team combines chemical ecology, the study of natural chemicals, and bioprospecting, the search for those chemicals in living tissue.

A certified diver, Baker collected tunicate specimens more than 100 feet below the surface in waters that was 28 degrees Fahrenheit. Harvesting the animals was difficult, but Baker needed only a small amount of the compound for testing.

He made sure the National Cancer Institute got a large batch to study.

``Sometimes you're lucky to get a few milligrams of a substance,'' said Bob Schultz, an organic chemist with the institute's developmental therapeutics program. ``But in this case, Baker gave us more than 100 milligrams, so we have plenty of material to work with. If a natural product shows promise, it's good to have it in large quantities.''

The compound will require years of further study before it can be tested on animals, NCI officials said.

Reporter Kurt Loft can be reached at (813) 259-7570.
This story can be found at: http://news.tbo.com/news/MGB311RKN4E.html Comments (36)

Stress accelerates experimental skin cancer Posted Friday, December 31, 2004 by arjuna
Last Updated: 2004-12-29 14:31:21 -0400 (Reuters Health)

By David Douglas

NEW YORK (Reuters Health) - Mice exposed to stress and ultraviolet radiation develop skin cancer significantly faster than do animals exposed to radiation only, researchers have found. They suggest this may be relevant to people at high risk of skin cancer.

Dr. Francisco Tausk of the Johns Hopkins Medical Institutions, Baltimore, and colleagues irradiated restrained mice with ultraviolet B rays, and stressed the animals by exposing them to the odor of urine from foxes, which are natural predators of mice.

Stress exposure began 14 days before irradiation and continued three times a week for the duration of the study.

A comparison group of "control" mice were housed in another room and were irradiated without urine exposure.

The first tumor appeared in the stressed group after 8 weeks, but not in the control group until the 21st week, the team reports in the Journal of the American Academy of Dermatology. In addition, 35 percent of the stressed mice had at least one tumor compared with 7 percent of controls.

If these results can be applied to the problem of sun-induced skin cancers in humans, Tausk told Reuters Health, they suggest that "stress-reducing techniques could help to ameliorate the development of these tumors."

Possible approaches might include meditation and self-hypnosis. "Psychosocial interventions" have been reported in the past to prolong the lifespan of cancer patients, he added.
SOURCE: Journal of the American Academy of Dermatology, December 2004. Comments (11447)

Isolated-limb chemo curbs advanced melanoma Posted Friday, December 31, 2004 by arjuna
Last Updated: 2004-12-31 11:49:16 -0400 (Reuters Health)

NEW YORK (Reuters Health) - For people with advanced but localized melanoma, delivering potent chemotherapy to just the limb with the cancer is highly effective both in terms of local disease control and survival, Dutch clinicians report.

This approach, they say in the December Annals of Surgery, "should be considered in all cases of limb-threatening tumors or in situations where simple surgical procedures to obtain local control fail."

The technique involves clamping off the affected limb with a tourniquet, while maintaining circulation in the isolated region with an external pump similar to a heart-lung machine. The limb can then be perfused with very high concentrations of chemo drugs, notably with a powerful agent called tumor necrosis factor, TNF.

In their article, Dr. Dirk J. Grunhagen and colleagues from the Daniel den Hoed Cancer Center in Rotterdam report their experience with 100 TNF-based isolated-limb perfusions performed over a 12-year period in 87 patients with advanced melanoma

A complete response was achieved by 69 percent of the subjects and a partial response by 26 percent, with the remaining 5 percent having no change in their condition.

Side effects of the treatment were "mild to moderate in almost all cases," the team reports, "with no treatment-related death and one treatment-related amputation."

Overall, 55 percent of the patients experienced local progression of the melanoma after an average of 16 months, and the estimated survival after five years was 32 percent.

For people who had a complete response, the numbers were better, with local progression noted in 52 percent after an average of 22 months and a five-year survival rate of 42 percent.

At present, Grunhagen's team concludes, isolated limb perfusion with TNF is "the most efficacious" procedure for patients with limb-threatening melanoma that cannot be dealt with surgically.
SOURCE: Annals of Surgery, December 2004. Comments (392)

Cancer scare shows commissioner what matters in life Posted Sunday, December 26, 2004 by arjuna
msnbc.msn.com

Amid tough year, Selig finds perspective
Cancer scare shows commissioner what matters in life

Updated: 1:01 p.m. ET Dec. 25, 2004

On Election Day, baseball commissioner Bud Selig went to his doctor for his regular checkup. And, as usual, his physician Ian Gilson told him he was in "great shape," according to Selig. They chatted about Gilson's work for baseball in trying to establish new standards for steroid testing in the sport.

"I've got to keep you going great for another five years," joked Gilson. With that, the doctor sent the 70-year-old Selig, who has five years left on his contract, on his way.

But then Gilson stopped him.

"As I'm outside the door of the office walking away, my doctor called and said, 'Come back here. What's that on your face?' " Selig said.

Every morning when Selig looked in the mirror, he saw a blotch on the skin above his right eye. But like countless others, he ignored it.

"I had never been sick in my life," Selig said. "I had only been in the hospital once -- ever. Serious illness was something that happened to other people."

Selig went to a dermatologist the next day. Within three days, test results revealed the biggest shock of his life. "It was 12:30 p.m. on Nov. 5," said Selig. "The doctor said, 'I hate to give you bad news on a Friday.' "

The blotch was cancerous. Worse, it was Clark Level IV melanoma, which can mean that the disease has already spread through the lymphatic system and may be incurable and fatal.

"When I heard 'level four melanoma,' I was stunned," Selig said this week in his first interview about his two-month ordeal.

"I looked it up [in medical texts]. My kids did, too. It's not good."

"I was just, 'Ohhhhhhh,' " said Selig, like the breath had been sucked out of him.

Every day he worried. "One day I took three of my granddaughters shopping," Selig said. "I was so distraught that I sat in my car and cried."

Meantime, baseball seemed to throw a new crisis at him every day. Three days before he was scheduled for surgery, the BALCO scandal broke wide open while he was in Washington to welcome the nation's capital back into baseball after 33 years. The next day, Barry Bonds's grand jury testimony about using the "clear" and the "cream" led the national news.

Meantime, doctors had given Selig his odds. There was perhaps a 90 percent chance that the cancer had been caught before it spread. But that was just an educated guess. And the other 10 percent chance would be bad news.

On Dec. 6, Selig had three hours of surgery that included the removal of two lymph nodes. He also had plastic surgery and skin transplants. He was hospitalized at Memorial Sloan-Kettering Cancer Center in New York for three days.

"I thought I would be out of the hospital the next day," Selig said.

"My only thought was just to get it over. . . . Actually, I couldn't really believe I was there," Selig said.

"Wherever I went in the hospital, they wanted to talk baseball with me. My plastic surgeon is a Red Sox fan. So he said, 'Now I have to do a good job on you since we finally won.' "

However, the toughest time for Selig may have been the seven days between his surgery and the final clinical results.

"After they took out the two [central] lymph nodes, they said the margins around the nodes looked clear [of cancer]," Selig said. "But they had to do microanalysis. You know me. I'm a worrier anyway. Well, [for a week] I worried, I can tell you. I came to [the doctor's] office and waited for 20 minutes. I pace up and down when it's just the ninth inning of a ballgame. It felt like it took 20 hours for him to come out. He said some small talk thing and I blurted out, 'Well?' "

On Dec. 13, almost six weeks after his nightmare started, he finally got the definitive word he longed to hear.

"You're clear and clean as hell," said his surgeon, Ashok R. Shahan, according to Selig.

Selig was lucky and knows it. The whole experience left him shaken and Selig is sobered and eager that others understand the importance of regular checkups with attention to possible skin cancer. "Melanoma is everywhere," he said this week. "As soon as I got it, it seemed like everybody I met knew someone or had someone in their family who had also had it."

Now that he's had time to reflect, Selig says, "We need reminders of what is important. Take some vacation. Calm down." So, he's gone on holiday where he'll try not to worry about the latest convoluted twist in baseball in Washington or the Randy Johnson trade.

Still, Selig grasps the irony that, even when things seem to be going best, you can't let your guard down. Just six days before he heard the words, "Come back here. What's that on your face?" the commissioner was presenting the championship trophy to the Red Sox after one of the greatest seasons in baseball history.

All-time attendance records had just been broken and TV ratings were up. After a dismal period a decade ago when he took much of the blame for the Strike of '94, Selig had, in recent years, drawn praise for pushing major innovations, including interleague play, as well as a crucial labor settlement in '02 that finally brought a period of peace to the sport.

In fact, three of the past four champions, including the Red Sox, were wild-card teams -- a controversial change that Selig championed and, because of the current power of the commissioner's office, essentially brought into being.

Yet, just as everything seemed ideal, a serious cancer struck that was certain to spread if undetected.

"Everybody needs to be checked for skin cancer regularly. Why, I'm a guy who never even sat in the sun," said Selig, the boss of a summer sport who seldom even has a tan.

Now he's out in Arizona with family and says he expects to enjoy the holiday season even more than usual.

"But I guess I won't be wearing a baseball hat out there. I'll get one with a wide brim," Selig said. The commissioner gets quiet, thinking back to the split-second when his doctor had a hunch and called him back.
"I was two steps out the door," he says. Comments (497)

"What we really want is to come up with treatments for melanoma," Posted Sunday, December 26, 2004 by arjuna
msnbc.msn.com

Research yields clues to why hair turns gray
Mutated gene may cause premature graying, study finds
The Associated Press

Updated: 4:29 p.m. ET Dec. 23, 2004

WASHINGTON - Those annoying gray hairs that increasingly leer back from the bathroom mirror may have some value after all. Cancer researchers have developed a new explanation for graying hair that they hope will also shed light on the most dangerous type of skin cancer.

"Preventing the graying of hair is not our goal," said senior researcher Dr. David E. Fisher of the Dana-Farber Cancer Institute in Boston.

"What we really want is to come up with treatments for melanoma," Fisher said in a telephone interview. Melanoma is the malignant form of melanocytes, the cells that help color hair and skin, and it is particularly resistant to chemotherapy and radiation.

Fisher's team found that hair goes gray when melanocytes become depleted.

The scalp contains a reservoir of adult stem cells that provide a continuous supply of these color-making cells, they found. But as the body ages these cells become depleted and sometimes begin to develop in the wrong part of the hair follicle.

The research, published online Thursday by the journal Science, originally focused on mice. But the team also studied human scalp tissue at various ages and found a similar pattern of cell depletion.

It was known that the pigment was not well transferred into gray hair, but the actual mechanism had not been understood, Emi K. Nishimura, a co-author of the paper, said in a telephone interview.

Gene may predict gray hair She said a gene called Bcl 2 is essential to maintain melanocytes. The researchers found that when they raised mice lacking this gene the animals went gray quickly and dramatically shortly after birth.

Fisher suggested that people who get gray prematurely may have a mutation of this gene.

The question they now want to answer is why the melanocyte cells begin dying off as the body ages.

These cells are generally good at surviving, being able to live through ultraviolet radiation -- at the beach, for example -- that would kill many other cells. That can be good when people go to the beach because the melanocytes produce pigment that protects the skin.

Unfortunately, they retain that ability to survive when they become cancerous, Fisher said.

So, he said, the researchers wondered if they could find a back door to killing the cells by studying how they die naturally, and that's what led to their research on graying.

By understanding how genes like Bcl 2 protect the cells, what pathways they act on, Fisher said, the scientists can look for ways to block that action with a drug.

"We have a number of ideas ... the work is moving," Fisher said. "I cannot say that we have drugs in our hands, but we have targets."

The American Cancer Society expects about 55,100 people to be diagnosed this year with melanoma, the most serious form of skin cancer, with an estimated 7,910 deaths.

Melanoma can be cured when it is detected and treated early, but if the lesion penetrates deeply into the skin it is often fatal. Sun exposure is a major risk factor in the disease, which has been increasing in the past few decades.
The research was supported by the National Institutes of Health, the Charles A. King Trust of Fleet National Bank and The Medical Foundation. Comments (123)

I've heard there are cancer vaccines Posted Sunday, December 26, 2004 by arjuna
The Boston Globe
www.boston.com

I've heard there are cancer vaccines

December 21, 2004

If I get one, will it prevent cancer? M.B., Brighton

Unfortunately, no.

Although many cancer vaccines are being studied, so far, none has been approved by the US Food and Drug Administration, said Jeffrey Schlom, chief of the Laboratory of Tumor Immunology and Biology at the National Cancer Institute.

And when they are approved, they will be aimed not at preventing diseases, -- like the flu and polio vaccines -- but to keep cancer from coming back after treatment. Cancer vaccines are "therapeutic," designed to rev up the immune system to fight a cancer that's already present, or to keep the immune system primed to notice and fight any cancer cells that recur.

Vaccines have already been approved to treat cancers linked to viruses. There is a vaccine against hepatitis B, and an experimental vaccine against hepatitis C; both viruses are associated with liver cancer. And there is a promising vaccine in late-stage testing against HPV, human papilloma virus, which is associated with cervical cancer.

For the cancers not associated with viruses, researchers are designing vaccines to directly attack proteins called antigens on the surface of cancer cells. Sometimes, the same antigens pop up in diverse malignancies -- breast cancer, lung cancer, and colorectal cancer -- which means that the same vaccine could be used against all three. In other cases, cancer cells carry a unique antigen, which means a special vaccine would have to be developed just against that cancer. In still other cases, researchers are working on vaccines that would attack antigens unique not just to the cancer but to the particular person.

Among the more promising vaccines are those to fight melanoma, the deadly skin cancer, said Dr. Stephen Hodi, clinical director of the melanoma program at the Dana-Farber Cancer Institute. There are dozens of such melanoma vaccines in clinical trials, and one, Melacine, has been approved in Canada.
JUDY FOREMAN Comments (135)

Researchers eye drug to thwart melanoma cells Posted Sunday, December 26, 2004 by arjuna
bostonherald.com
By Brian Ballou Tuesday, December 21, 2004

Local researchers announced yesterday they may have found a way to stop the growth of deadly melanoma cells in humans, a breakthrough that may unlock treatments for other forms of cancer.

``This is exciting because it focuses on the precise pathways that are driving the cancer cells,'' said Dr. David E. Fisher, director of the melanoma program in medical oncology at the Dana-Farber Cancer Institute and Harvard Medical School.

Since 2002, Fisher and other researchers at the institute and at Children's Hospital Boston have been busy trying to figure out how to combat the skin cancer melanoma, focusing on a protein called CDK2. They discovered melanoma can't grow without a steady supply of that protein.

By using drugs that cut off the supply of CDK2 to melanoma cells, they hope to beat back the cancer, which claims thousands of lives every year. Normal cells don't need CDK2, Fisher said.

``This may be a unique opportunity to not only understand the problem but aim a drug at that problem,'' Fisher said.

Shonda Schilling, the wife of Red Sox pitcher Curt Schilling, was diagnosed with melanoma in 2001. A year later, she created The Shade Foundation, with a goal to educate society about sun exposure. Melanoma has been linked to prolonged sun exposure.

``I welcome all efforts to prevent and cure malignant melanoma as the mother of four young children and in a high-risk family,'' she said from her home in Arizona.

So far, the breakthrough has occurred only in a petri dish. Clinical tests on humans are needed. Pharmaceutical companies are working to develop a CDK2-inhibitor, Fisher said. ``As soon as we found out about this, we were on the phone to the drug companies,'' he said.
According to the American Cancer Society, more than 55,000 people were diagnosed with melanoma in the United States this year. Melanoma is responsible for about 7,900 deaths this year in the United States, and the death toll is expected to rise in 2005.
Comments (62)

Skin cancer: Children beware Posted Tuesday, December 7, 2004 by arjuna
News24.com 30/11/2004 11:10 - (SA)

Sydney - Australian children as young as three have been found to suffer potentially cancer-causing changes to their skin due to sunlight, according to a new study issued Tuesday.

The study by the Queensland Institute of Medical Research showed a strong link between exposure to sunlight and development of potentially cancerous moles in young children.

Children exposed to the sun had developed at least 10 moles by the time they reached the age of three, the study found.

"These are very high rates of moles and moles are the biggest risk factor for developing melanoma," said researcher David Whiteman, referring to the deadliest form of skin cancer.

"This is the first evidence we have seen in very young children that protective measures actually do work to stop the early changes of skin cancer.

"It's not proven yet but it does seem that sun exposure received during childhood is more dangerous than sun exposure received during adulthood."

The results are to be published in January in the journal of the American Academy of Dermatology.
Edited by Tori Foxcroft Comments (275)

Addition Urged for Melanoma Memory Device Posted Tuesday, December 7, 2004 by arjuna
Know your ABCDEs to detect cancer, researchers suggest

By Steven Reinberg HealthDay Reporter

TUESDAY, Dec. 7 (HealthDayNews) -- An alphabetical mnemonic that dermatologists give to their patients to help identify melanoma, the most virulent form of skin cancer, needs a simple addition, researchers say.

When melanoma is caught and treated early, the survival rate can be as high as 96 percent. So it pays to look at the moles on your skin closely for any signs of cancer. One simple way of knowing when moles may be cancerous is the ABCD system, which has been used since 1985.

In the system, "A" stands for asymmetry, where one half of a mole doesn't match the other half. "B" is for border irregularity, where the edges are ragged, notched or blurred. "C" is for color that is a nonuniform mixture of brown, black, red, white or blue. And "D" is for diameter, especially when the mole is bigger than 6 millimeters, about the size of a pencil eraser.

Now researchers are recommending that "E," for evolving, be added to the list. An evolving mole is one that is changing in size, shape, and symptoms -- such as itching or tenderness, surface bleeding, or shades of color, according to their report in the Dec. 8 issue of the Journal of the American Medical Association.

There will be more than 50,000 new cases of melanoma diagnosed in the United States each year, according to the American Cancer Society, and more than 7,000 will die from the disease.

"This ABCD acronym has been in place for almost 20 years," said lead researcher Dr. David Polsky, an assistant professor of dermatology at New York University Medical School. "We decided to review the medical literature on the utility of the ABCD acronym."

After the review, Polsky and his team are recommending that E for evolving be added to the ABCD acronym.

"This recognizes the changing nature of melanomas," he said. "We want to recognize that more, because we think that this is a very critical element of melanomas. We want the public to pay more attention to changing moles."

One type of melanoma, called nodular melanoma, represents about 15 percent of this form of cancer, Polsky explained. "Nodular melanomas don't have the ABC characteristics, but they tend to grow rapidly," he added.

By adding "E" to the acronym, Polsky hopes these melanomas can be diagnosed earlier. "Oftentimes because they don't have the ABC characteristics, they're diagnosed at a more advanced stage. Since nodular melanoma is an aggressive form of cancer, we wanted to emphasize the changing nature of melanoma in general, and hope that this would capture nodular melanomas earlier," Polsky explained.

"People should be examining their skin periodically," Polsky said. "Lesions that are changing should be brought to the attention of their doctor."

"The authors have previously made a tremendous contribution to melanoma awareness and earlier diagnosis with their ABCD criteria," said Dr. Jeffrey Salomon, an assistant clinical professor of plastic surgery at Yale University School of Medicine. "Make no mistake about it, that contribution has translated into countless lives saved."

However, Salomon cautions that the epidemic of melanoma continues and doctors and their patients must be on the lookout for this deadly cancer. "The addition of E is another critical stone in the wall that separates more reliably screened people from less reliably screened people. The recommendation is timely and should be well received and appreciated by physicians and the lay public alike," Salomon said.

Not everyone agreed with that assessment, though.

"I think that it [adding E] is a poor suggestion," said Dr. Martin A. Weinstock, a professor of dermatology and community health at Brown University and chairman of the American Cancer Society's Skin Cancer Advisory Group.

Weinstock believes that the current ABCD criteria describes some but not all melanomas. However, tinkering with it only adds confusion, he said.

"The most important warning sign for melanoma is change in size, shape or color of an existing mole," Weinstock said. And one should not worry about whether it meets the ABCD criteria. "ABCD can be noted as a description of some melanomas, but certainly not all."

More information

Get a primer on skin cancer from the American Cancer Society .
SOURCES: David Polsky, M.D., Ph.D., assistant professor, dermatology, New York University Medical School, New York City; Jeffrey Salomon, M.D., assistant clinical professor, plastic surgery, Yale University School of Medicine, New Haven, Conn.; Martin A. Weinstock, M.D., Ph.D., professor, dermatology and community health, Brown University, Providence, R.I., and chairman, American Cancer Society Skin Cancer Advisory Group; Dec. 8, 2004, Journal of the American Medical Association Comments (222)

Chemo technique can curb some melanomas Posted Monday, November 22, 2004 by arjuna
Last Updated: 2004-11-22 15:39:30 -0400 (Reuters Health)

NEW YORK (Reuters Health) - When malignant melanoma on an arm or leg advances it may become impossible to remove surgically, even if the cancer hasn't spread to other areas of the body. In such cases, chemo delivered just to the affected limb offers a good treatment option, Dutch doctors report.

Their study shows that more than half of patients with locally unresectable melanoma achieve a complete response after so-called isolated limb perfusion with the chemo drug melphalan (abbreviated to M-ILP).

"Half of these patients are rendered disease-free for a long time," Dr. Eva M. Noorda, at Slotervaart Hospital in Amsterdam, and her colleagues report in the Archives of Surgery for November.

Noorda's team reviewed the outcomes of 108 patients with unresectable melanoma who underwent a total of 130 M-ILP treatments. The procedure involves clamping off circulation to the affected limb for an hour during which time perfusion is maintained using an external machine while the chemo is added to the oxygenated blood artificially circulating through the limb.

A complete response lasting an average of 10 months was attained in 72 (55 percent) of the 130 M-ILPs performed.

Whether the cancer had spread to lymph nodes was the only factor that affected the chances of a complete response and lack of recurrence in the affected limb. Otherwise, factors such as the site of the tumor, its thickness, or the number of tumors did not significantly affect outcomes.

After an average follow-up period of 21 months, only four patients required limb amputation, the researchers report.

Among patients who had a complete response, average survival was 44 months, compared with 15 months otherwise.

"Maximum efforts should be made to obtain a complete response," Noorda's group writes, "although the response to isolated limb perfusion is probably partly dictated by the biological features of the disease in the individual patient."
SOURCE: Archives of Surgery, November 2004. Comments (0)

The hidden risk in your family tree Posted Tuesday, November 16, 2004 by arjuna
TARA PARKER-POPE, The Wall Street Journal
Tuesday, November 16, 2004

(11-16) 08:00 PST (AP) --

Cancer risk can lurk in some surprising places in the family tree.

About 10 percent of common cancers are the result of heredity, but sometimes the risk isn't obvious. Many women, for instance, think they are at risk only if their mother's family had breast cancer and don't realize paternal risk plays just as much of a role. Similarly, if a man's family has a high incidence of breast cancer, it could increase his risk for prostate cancer. A family history of ovarian cancer may also increase a man's risk for melanoma, prostate or colon cancer.

Indeed, many seemingly unrelated cancers -- such as melanoma and pancreatic cancer or colon and endometrial cancer -- sometimes share a common genetic thread. But despite the revolution in genetics under way, hereditary risk for cancer often goes undetected. Fewer than one-third of patients have assessed their family health history, according to a report published last week by the Centers for Disease Control. In a bid to increase awareness of the link between family history, cancer and other diseases, the surgeon general has declared Thanksgiving Day "Family History" day, urging families to talk about their health in between helpings of turkey and pumpkin pie.

Even though most cancer isn't genetic, tracking down the people who do have genetic risks will go a long way toward catching and even preventing many cancers earlier, because people at known risk will be able to seek more aggressive screening and monitoring. Even a single case of cancer at an early age in the family, such as breast cancer before 45 or colon cancer before 50, should prompt a trip to a genetic counselor.

Genetic risk is so complex and confusing that even many doctors get it wrong. That was the case with 69-year-old Samuel Tauster, a Manalapan, N.J., chemist whose mother and cousins all died of breast cancer at an early age. After doctors told family members that breast-cancer risk could be passed only from mother to daughter, he didn't think his own children had to worry.

Later, he learned the doctor had been wrong. As a result, earlier this year, Mr. Tauster, his brother and sister were all tested for BRCA, a genetic mutation that triggers breast cancer in 50 percent to 85 percent of women who carry it. Mr. Tauster and his brother both tested positive for the mutation, and later so did his two daughters and his niece.

All three women opted for surgery to remove both breasts and ovaries as a preventive measure. "If I knew I was at high risk I would have been getting checked more often," says Mr. Tauster's 44-year-old daughter, who asked not to be named. "But nobody thought I was at risk because it was on my father's side."

BRCA mutations have been linked with melanoma, prostate, gall-bladder, colon, pancreatic and male breast cancers. Alison Estabrook, chief of breast surgery at St. Luke's Roosevelt Hospital in New York, says she recently saw a 36-year-old patient whose father and paternal grandfather both died of prostate cancer. The woman, as well as her two sisters, tested positive for BRCA. "If your father had colon or prostate cancer in his 40s, that might be a reason to be tested," says Dr. Estabrook. "But most people wouldn't link that with breast or ovarian cancer."

Researchers have identified several other hereditary links to cancer, although most are relatively rare. At least six genetic mutations are linked with hereditary risk for colon cancer, but families with the genes may also have higher rates of endometrial, ovarian, stomach, kidney, thyroid and childhood liver cancer. Rarely, pancreatic cancer may be linked to one of four genes that increase risk for melanoma. A family history of sarcoma can signal a genetic risk for melanoma, leukemia, breast, brain and adrenal cancers.

Figuring out whether there's a genetic link between cancers in your family is virtually impossible to do on your own. Seemingly obvious patterns, such as a high occurrence of melanoma in one family, may be misleading. While skin cancer appears to run in families, the reason often isn't genetic. The pattern instead may be due to the fact that the entire family regularly spent summers at the beach and everyone was exposed to the same harmful rays, says Peggy Cottrell, a New York genetic counselor who works with Dr. Estabrook.

To be sure that cancer isn't in your genes, the best bet is to talk with a genetic counselor. A risk assessment costs between $125 and $300 and likely will be covered by insurance with a doctor's referral. In addition to early-age cancer in the family, other reasons to discuss risk for carrying a gene include male breast cancer, ovarian and breast cancer in the same family, or any unusual cancers or clusters of a single type of cancer.

A genetic counselor will also want details about how the disease affected family members and where it occurred. Cancer found in both breasts or both kidneys, for instance, may be more significant than an occurrence on one side of the body. A melanoma lesion on the tip of the nose suggests the disease is due to sun exposure, while melanoma on the sole of the foot may signal a hereditary syndrome, triggering further testing.

Many people who seek genetic counseling are reassured that their risk is the same as everyone else's. But for those who go on to get tested for a cancer gene, insurance typically pays for the blood work, which can cost between $750 and $3,000, depending on the gene being studied. Even if a gene isn't identified, it's possible that a genetic risk still exists but the unique mutation wasn't found by the test. As a result, those who test negative for a cancer gene are often advised to undergo regular screening and monitoring, says Dawn C. Allain, ex-president of the National Society of Genetic Counselors and a genetic counselor at Waukesha Memorial Hospital in Waukesha, Wis.

As part of the surgeon general's initiative on family health history, the Department of Health and Human Services has launched a new Web tool at www.hhs.gov/familyhistory that allows you to track family health patterns that might signal higher risk for cancer or other diseases. The National Society of Genetic Counselors offers a database at www.nsgc.org/resourcelink.asp that helps you find a genetic counselor in your area. Comments (0)

Link between immune protein and longer survival in melanoma patients identified Posted Friday, November 5, 2004 by arjuna
eurekalert.org/public news

CHARLOTTESVILLE, Va., Nov. 4, 2004 -- Immune responses to prevent or delay the spread of melanoma, a deadly form of skin cancer, are more likely to prolong survival in patients if their immune cells carry a special kind of marker on the surface, according to a team of researchers at the University of Virginia Health System. The finding is published in the November 1 issue of the journal Cancer Research, found on the web at http://cancerres.aacrjournals.org/

The researchers correlated the presence or absence of the protein with survival in 52 U.Va. patients with advanced metastatic melanoma who were enrolled in experimental clinical trials over the last decade. They found that survival increased by fifty percent in patients whose T lymphocytes (the immune cells that kill tumors) carried a particular protein, or chemokine receptor, called CXCR3.

Increased survival was seen in patients with Stage III metastatic melanoma, but no increased survival was noticed in patients with Stage IV, stressing the importance of early detection and treatment for melanoma.

"As immunologists continue to target the spread of cancer, this research gives scientists new clues to help develop vaccines that both 'turn-on' cancer-killing immune cells, as well as instruct the cells on how to find tumors. Together, that will improve the efficacy of vaccines against cancer in the future," said the study's principal investigator David W. Mullins, PhD, assistant professor of microbiology and a researcher in the Human Immune Therapy Center (HITC) at the U.Va. Health System.

The idea behind this type of vaccine is to activate an immune response within the body against melanoma. In the past, Mullins explained, physicians have delivered vaccines that can get lost in the circulatory system. But, researchers can now target vaccines to certain lymph nodes in the body that they know will generate T cells with the appropriate chemokine receptor like CXCR3- a 'homing' feature that allows these killer cells to find and eradicate tumors.

"This data may indicate that early melanoma vaccination is essential, and that vaccines inducing specific T cells with tumor-homing ability can make a significant difference in survival," said study co-author Irene Mullins, an instructor in the Department of Health Evaluation Sciences at U.Va.

"With lung disease for example, where surgery may not be an option, vaccines offer a treatment alternative to prolong the lives of patients," David Mullins said. "Something as simple as the induction of a particular chemokine receptor on T cells can translate into enhanced survival, which can be quite profound."

The discovery was made possible because of a unique combination of resources at the U.Va. Health System, including collaboration between laboratory scientists, clinicians and statisticians. David Mullins stressed that the organization of the Human Immune Therapy Center at U.Va. means that research can be brought from the lab to the clinic in a matter of days, rather than months or years. "We are quickly retargeting vaccines at U.Va. to be used in patients, taking advantage of our observations," Mullins said.

Last year, Dr. Craig Slingluff, professor of surgery at U.Va. and director of the HITC, reported that using molecules called peptides to treat melanoma resulted in an immune response from 75 percent of the patients in a phase II clinical trial of a melanoma vaccine. The vaccine was also associated with tumor regression.

Comments (0)

Surgeons Identify Possible Mechanism for Cancer Metastasis to the Liver Posted Monday, October 11, 2004 by arjuna
Yahoo.com/news

NEW ORLEANS, Oct. 11 /U.S. Newswire/ -- Surgeons from the John Wayne Cancer Institute, Santa Monica, CA, have identified what may be a key mechanism by which cancer metastasizes to the liver, according to a study presented at the 2004 annual Clinical Congress of the American College of Surgeons (ACS). Results from the study show that the chemokine receptor CXCR4 genes--typically quiescent or downregulated in normal cells, is in liver metastases from patients with colorectal cancer and melanoma. CXCR4, usually found on immune cells, was shown not only to be present on cancer cells but also to be functional. When cancer cells bearing the CXCR4 receptor were stimulated by the protein (CXCL12) that binds to them, there was a significant increase in cell migrational activity.

"We know that other factors for cancer metastasis exist, but we think CXCR4 may play a major role in liver metastasis. By our initial analysis, we found that this was the most common chemokine receptor in patients with colorectal cancer and melanoma liver metastasis," Joseph Kim, MD, a fellow in surgical oncology at John Wayne Cancer Institute, said. Chemokine receptors typically play a critical role in orchestrating immune cells to specific sites during immunologic response; it appears that cancer cells use this same mechanism.

Further research could lead to the development of drugs that target the CXCR4 receptor to treat cancers that metastasize to the liver. Cancer cells that metastasize to the liver may bear the CXCR4 chemokine receptor, so they can be an alternative target for therapy. "Industry is currently producing methods to specifically target cancer cells by targeting the CXCR4," Dr. Kim said.

Because most patients with cancer can die from distant organ metastasis, there has been a focus to determine why or how cancer spreads to specific organ targets. One theory, known as the homing or signaling mechanism, relies on the activities of receptors on the surface of malignant cells. Dr. Kim's research on the CXCR4 receptor provides some support for that theory. "CXCR4 is a specific receptor for one particular protein (CXCL12), which is highly produced by the liver. It supports the signaling or homing hypothesis in that the cells that have this receptor will aim for or migrate toward the organ that produces the highest level of the protein, such as the liver," he explained.

Researchers from other institutions have shown that chemokine receptors affect metastasis in cell cultures and animal studies. Dr. Kim and his associates wanted to determine whether the chemokine receptor CXCR4 influenced metastasis in patients with cancer. "Our focus was to find out whether there actually was clinical relevance and similarity of function for chemokine receptors of melanoma and colorectal cancers that metastasize to the liver," Dr. Kim said.

In a previous study, presented at the 2004 meeting of the American Society of Clinical Oncology (news - web sites ), Dr. Kim showed that there was significant upregulation of CXCR4 in liver metastases from patients with colorectal cancer. Among patients with stage I or II colorectal cancer in this study, 30 percent who had high CXCR4 expression developed local or distant metastasis. However, none of the patients with low expression of the chemokine receptor showed signs of metastasis after 39 months of follow-up.

In the study reported at the 2004 annual ACS Clinical Congress, Dr. Kim and his associates focused on melanoma as well as colorectal cancer. "We thought if the chemokine receptor aided in colorectal cancer metastasizing to the liver, it might promote metastasis in other cancers. So we looked at colorectal cancer and melanomas to see if the same mechanism for two completely different cancers led to or aided in forming liver metastasis," he explained.

The study used microarray technology, which assesses multiple genes in a single experiment, to screen for the presence of chemokine receptors on the surface of cancer cells in liver metastasis samples from patients with melanoma and colorectal cancer. This analysis revealed that CXCR4 was the most commonly expressed chemokine receptor by both cancers. CXCR4 was expressed in 13 of 16 tumor specimens from patients with melanoma metastasis and all 22 specimens from colorectal patients with liver metastatic disease.

The researchers then assessed how the CXCR4 receptors functioned on cancer cells by treating cancer cells with the protein that binds to the CXCR4 receptor, CXCL12 (stromal cell- derived factor-1, (SCDF-1) ), and then measuring cellular migrational activity. "Just having a receptor doesn't necessarily mean that it actually does something. So we wanted to establish that the receptors on the cell surfaces were functional. We found that higher numbers of cancer cells responded to the protein than control cells," Dr. Kim said. The rate of response to CXCL12 was greater in melanoma and colorectal cancer cells than in control cells. "This finding shows that the protein leads to a transformation in the cell machinery," he explained.

Dr. Kim and his colleagues are conducting further studies to learn how the CXCR4 chemokine receptor may be altered by environmental factors. He also is trying to determine if the receptor is expressed by other liver metastases. "CXCR4 may play a role in the mechanism of metastasis for not only melanoma and colorectal cancer. It may be important for all cancers that metastasize to the liver," he said.
Also participating in the study were Takuji Mori, MD, PhD; Stella Lam, BS; Lonnissa Nguyen, BS; Donald Morton, MD, FACS; and Anton Bilchik, MD, PhD, FACS. The study was supervised by Dave SB Hoon, PhD. = Comments (2)

A comparison of dermatologists', surgeons' and general practitioners' surgical management of cutaneous melanoma Posted Saturday, October 9, 2004 by arjuna
D.B. McKenna J.C. Marioni R.J. Lee R.J. Prescott V.R. Doherty

British Journal of Dermatology

Abstract

Background

Current guidelines for the surgical management of melanoma aim to bring a combined consensus approach to the surgery of melanoma. Whether different outcomes for melanoma are related to the specialist who treats the patient is unknown.

Objectives

To examine the clinicopathological features and surgical management of patients with primary cutaneous malignant melanoma treated by dermatologists, general surgeons, plastic surgeons and general practitioners (GPs). We also examined if the category of specialist had an effect on the survival outcome for the patient.

Methods

A retrospective, observational study of patients registered on a specialist database that records the clinicopathological features, surgical treatment and follow-up information of patients with malignant melanoma in Scotland. The patients had invasive primary cutaneous malignant melanoma without evidence of metastasis at the time of surgery, diagnosed between 1979 and 1997, with follow-up to the end of December 1999. Clinicopathological characteristics and surgical treatment of patients were compared for the four groups of specialist, as were overall survival (OS), disease-free survival (DFS) and recurrence-free interval (RF).

Results

Of 1536 patients, 663 (43%) were treated initially by a dermatologist, 486 (32%) by a general surgeon, 257 (17%) by a plastic surgeon and 130 (8%) by a GP. The proportion of patients managed by dermatologists rose over the lifetime of the study. Compared with the other specialists, the patients treated by general and plastic surgeons were older; a higher proportion of female patients was managed by dermatologists; median tumour thickness, lesion diameter and frequency of ulceration were all greater in the general surgeon-treated group; plastic surgeons treated a higher proportion of lentigo maligna melanomas; and general surgeons and GPs saw a higher proportion of nodular melanomas. Over 90% of patients managed by a dermatologist or GP underwent wider local excision following initial excision, compared with 43% and 25%, respectively, in the general and plastic surgery groups. General surgeons used wider excision margins than the other specialists. OS, DFS and RF were significantly better in the dermatology group compared with the general and plastic surgery groups.

Conclusions
This study showed that dermatologists manage an increasing majority of melanoma patients and that there were significant differences in the surgical treatment of melanoma between dermatologists and surgeons. Survival was significantly better in the dermatology-treated group, suggesting that dermatologists should have a central role in melanoma management. Article Type: Original Article Page range: 636 - 644 Comments (0)

Sneaky Melanoma Posted Saturday, October 9, 2004 by arjuna
Prevention.com
9/29/04

African-Americans need to be on the alert for this cancer

by Doug Dollemore

The deadliest of skin cancers--melanoma--isn't just a threat for the fair-skinned. It's even deadlier for African-Americans, perhaps because neither doctors nor patients are expecting it. Here's how to stay safe.

Know that it's sneaky. Nearly two-thirds of melanomas among African-Americans occur in areas that get little sun exposure, including feet, palms, toenails, the inside of the mouth and nose, and, in women, the genitals. If you notice an odd mark, see your doctor right away.

Protect yourself. Wear sunscreen, long sleeves, and a hat. In addition, examine your skin from head to toe every month. Look for deep-black spots on skin, and deep-black streaks on nails. Ask your family doctor or dermatologist to check all potential trouble spots annually.

Push for treatment. With early intervention, melanoma has a 95 percent cure rate.
Doug Dollemore is a freelance health writer. Comments (0)

Arsenic exposure linked to melanoma risk Posted Saturday, October 9, 2004 by arjuna
Last Updated: 2004-10-07 14:43:27 -0400 (Reuters Health)

NEW YORK (Reuters Health) - Chronic exposure to arsenic, which can be measured in toenail clippings, seems to be associated with an elevated risk of melanoma skin cancer, investigators report.

"There has been little research investigating the link between arsenic and cutaneous melanoma, although arsenic has been associated with increased risk of nonmelanoma skin cancer." Dr. Lara E. Beane Freeman, of the National Cancer Institute, Bethesda, Maryland, and colleagues write in the October issue of the American Journal of Epidemiology.

The researchers looked for any association between melanoma and environmental arsenic exposure in 368 Iowa residents with melanoma and 373 with colorectal cancer. The participants completed a mailed survey, and submitted toenail clippings for analysis.

Arsenic accumulates in hair and nails and provides an indication of long-term exposure. The team analyzed the clippings for arsenic content by incinerating them in a graphite oven and measuring the proportion of elements by atomic absorption spectrometry.

Patients with the highest toenail arsenic concentrations were more than twice as likely to have melanoma as those with the lowest concentrations The risk was not related to skin color, skin type or history of sunburn.

"The association we observed with arsenic is not known to have been previously reported," the researchers note. "Therefore, the findings warrant confirmation."
SOURCE: American Journal of Epidemiology, October 2004. Comments (2)

Melanoma screening in Gozo Posted Saturday, October 9, 2004 by arjuna
The Malta Independent Online - News

------------------------------------------------------------------------ Web posted at 7:00 am CET October 9, 2004 ------------------------------------------------------------------------
-

The study of incidence of melanoma in Gozo, which was announced earlier this year, began last Saturday with the residents of San Lawrenz. The study is the first of its kind worldwide, as it screens a whole population, aged 16 and over, for melanoma incidence.

Melanoma is a deadly cancer of the skin with an incidence of 12-15 cases per 100,000 people. Considering that advanced cutaneous melanoma is still incurable, and it is increasing in many

countries, early detection is an important step towards a reduction in mortality.

Diagnosis in Gozo is carried out through a computerised system using imaging and completely non-invasive techniques.

In 1987, Italians Prof. Marco Burroni and Dottoressa Dell'Eva launched an innovative system for the early diagnosis of malignant melanoma, based on visual accuracy and artificial intelligence. DBDermo-Mips is based on a computer-linked dermatoscope that enables assessment of certain characteristics of pigmented lesions that are not visible to the naked eye, thus providing a valuable ancillary diagnostic aid to the dermatologist. Prof Lucio Andreassi, together with his team in Siena, perfected the discipline of digital epilumeniscence utilising this modern technology. Today, DBDermo-Mips is able to offer diagnostic results in seconds, with an accuracy of well over 90 per cent, resulting in earlier diagnosis which may mean the difference between cure and certain death.

The system is able to automatically analyse the spot under evaluation in real time and compare the values with a huge database of 145,000 digitalised images of all variants of melanoma, at a rate of 15 lesions per second. In this way the clinician focuses on the lesion and the system automatically gives its probability of malignancy by a beeping sound on a hand-held computer.

Gozo residents are being contacted by their respective local councils. The first group of residents that launched the project were those from San Lawrenz. It is planned that residents from the smaller villages will be checked first, gradually covering the entire population of the island in a three-year period.
The screening programme is being carried out by the Maltese Association of Dermatology and Venereology and the Gozo General Hospital (Ministry for Gozo). Comments (2)

Pfizer-Medarex deal aims to produce dozens of antibody-based drugs Posted Saturday, October 2, 2004 by arjuna
NewsDay.com
By LINDA A. JOHNSON AP Business Writer

September 20, 2004, 6:01 PM EDT

TRENTON, N.J. -- Pfizer Inc. is teaming up with a small biopharmaceutical company on long-term research in a promising area: making medicines using special antibodies that hone in on targets such as cancer cells and infections.

Medarex Inc. said Monday the 17-year-old company could receive more than $500 billion from Pfizer over a decade if the New York-based drug giant is able to turn antibodies produced by Medarex's genetically engineered mice into many successful drugs.

Shares of Princeton-based Medarex shot up as much as 17 percent on the news, then closed up $1.01, or 14.8 percent, at $7.84 on the Nasdaq stock exchange Monday. Pfizer shares dropped 73 cents, or 2.3 percent, to $30.99 in trading on the New York Stock Exchange. Both stocks saw heavy trading.

"It's a very significant deal for Medarex," partly because of the immediate cash infusion, said biotech analyst Brian Rye of Janney Montgomery Scott LLC.

"Psychologically, it's also important because for a small company such as Medarex, with no approved drugs on the market yet, to have the likes of Pfizer, the world's largest pharmaceutical company, make such a significant investment in your technology," he added.

Under the deal, Medarex faces no costs or financial risks and gets an initial cash payment of $80 million. Pfizer also will immediately buy about 6 percent of Medarex stock, or about 4.8 million shares, at $6.21 each. That was a slight premium over the trading price when the deal was hammered out last week, said Donald Drakeman, Medarex president and chief executive officer.

The big payoff could come down the road.

Over the next 10 years, New York-based Pfizer will try to find and develop up to 50 antibody-based drugs using Medarex technology. Including payments to cover research costs, license fees and milestone fees, Medarex would receive more than $400 million if all 50 products are approved, then would receive royalties in the 3 percent to 5 percent range on any sales, Drakeman said.

The technology involves special mice, genetically engineered by Medarex, so they have human genes that can tell their bodies to spew out many copies of human antibodies to attack substances injected into them, such as tumor cells.

That means any drugs Pfizer made from antibodies produced by Medarex, when given to a patient to fight disease, would not be rejected by the person's immune system, Drakeman said.

"The world's leading pharmaceutical company has decided that monoclonal antibodies are really an important part of their pipeline for the future," Drakeman said of Pfizer.

Pfizer would pick the diseases for which it would try to develop antibody-based drugs, but cancer is clearly a leading area.

Both companies have their own programs to develop a drug that would essentially rev up the body's immune system by blocking a molecule that functions as the system's emergency break. Medarex has a version, called MDX-010, that is in final-stage testing in people with late-stage melanoma, for which there is little treatment.

The two companies are retaining individual rights to develop their own products for the target.
While the partnership is a milestone for Medarex, it already has deals with other heavy hitters in the pharmaceutical industry using its mouse technology, including Johnson & Johnson, Eli Lilly and Company, Novartis Pharmaceuticals Corp. and Amgen Inc. Comments (0)

Cancer victim's message for all: Melanoma can strike anywhere Posted Saturday, October 2, 2004 by arjuna
The Detroit News
September 29, 2004

When you’re in your teens or 20s, you think you’re immortal. Cancer is something that happens to older people.

Angela Guenther was no different.

“No one believes this will ever happen to them, that they’re invincible. I thought that too,” she said when I first wrote about her in June.

But the 23-year-old Central Michigan University student learned it could happen to her. A large black mole with uneven edges her mother spotted on Angela’s back was diagnosed as melanoma, the most serious form of skin cancer.

This year, more than 55,000 Americans will be diagnosed with the disease.

Angela’s life turned into surgeries, radiation treatments and long weeks in the hospital. Her wedding was planned for June 2003. Just a week before the ceremony, she was able to leave the hospital.

“It was so wonderful to be able to get her to that point,” says her mother, Mary Jo Sights of Lake Orion. “It meant so much to her. But it was so scary as to where it was going to go from there.”

Angela wanted more than just a wedding. She wanted to buy a house and have a baby.

But melanoma was winning. The tumors were spreading across her body and into her brain.

Angela wasn’t willing to give up. She wanted to be the matron of honor at her sister’s wedding in August. Somehow, she made it. It was a beautiful day.

“Even though Angela was extremely ill and was really having a hard time, she was her matron of honor, and she was there,” says family friend Roz Mermell. “She made it.”

But this past week, beautiful Angela lost her fight.

Among her last e-mails was this one: “Remember how important life is and to live every day to the fullest, because you never know how long you are going to be here. I would love to stay alive and be with my husband and kids and live forever. So I am praying to just keep fighting and never giving up hope.”

Her mother e-mailed me, as well, and asked that I share her message:

“When people think of angels, I want them to remember Angela. ... People need to know that melanoma is a devastating disease without a cure. ... They need to know that sun block expires and to check the dates. They need to know that sunshine is best enjoyed in your heart, not on your body. Wear hats and sun block and protection, all the time, daily. ... Look carefully at moles or odd colorations on the skin and get immediately to a qualified dermatologist for evaluation. Don’t wait. Melanoma doesn’t.”

Angela and her mother spent these last months reminding people of the dangers of the sun.

“Everybody says it’s so important to be so tan,” her mother says. “It’s not. It’s important to live.”
Though Angela is gone, her family is left with thousands of dollars in medical bills they can’t afford. Comments (0)

Breast Cancer Associated With Melanoma Risk, and Vice Versa Posted Saturday, October 2, 2004 by arjuna
NEW YORK (Reuters Health) Sept 22 - There appears to be a bidirectional association between female breast cancer and cutaneous melanoma, according to results of a new study. While the finding might be confounded by increased surveillance in the two diseases, it does support increasing evidence of an overlapping genetic pathway.

"Epidemiologic studies have provided suggestive evidence of a link between cutaneous melanoma and breast cancer," Dr. Hensin Tsao, of Massachusetts General Hospital, Boston, and colleagues write in the September 20th issue of the International Journal of Cancer.

"Moreover," they point out, "carriers of mutations in the breast cancer predisposition gene, BRCA2, have an increased risk of melanoma while carriers of mutations in the melanoma susceptibility gene, CDKN2A, exhibit a higher than expected risk of breast cancer."

The researchers examined whether female breast cancer survivors in the Surveillance, Epidemiology, and End Results (SEER) database have an increased risk for melanoma, and vice versa. The team compared the expected number of cases to the observed number of cases.

Survivors of melanoma had an 11% increased risk of developing breast cancer. The risk was higher in patients diagnosed with melanoma at or before age 50 years (19% increased risk), those diagnosed more recently (17% increased risk), and for the first 3 years after the melanoma diagnosis (25% increased risk).

Overall, the risk of developing melanoma was increased by 16% in female breast cancer survivors. Younger patients (up to 50 years old) had a 46% increased risk of melanoma, while those who had undergone radiation therapy had a 42% increased risk.

"The elevated risk for cutaneous melanoma, especially among younger breast cancer patients, suggests that the genetic observations from high-risk groups may also be operative at a much lower level in the general breast cancer population," Dr. Tsao and colleagues conclude.

Int J Cancer 2004;111:792-794.

Comments (0)

Coley Pharma raises $25M to advance drug compounds Posted Saturday, October 2, 2004 by ctustis
Boston Business Journal

Coley Pharmaceutical Group Inc. has raised $25 million in new venture
financing to help support ongoing clinical development of its
anti-cancer and anti-virus compounds.

This is the fourth funding round for the company, which had raised over
$102 million in venture funding as of August 2003.

Existing investors participated in the round, including Thomas, McNerney
& Partners of New York, Venrock Associates of Cambridge, Menlo Park,
Calif., and New York; and Techno Venture Management of Boston and
Munich, Germany.

Coley's lead drug, ProMune, is in Phase II, or mid-stage clinical trials
to treat forms of lung cancer, melanoma and lymphoma. A separate
compound, Actilon, is in early-stage, or Phase I human clinical trials
to treat hepatitis C.

Coley last week announced a $16.9 million five-year contract with the
National Institute of Allergy and Infectious Diseases to develop new
compounds that activate the immune system to counteract bioterrorism.

Earlier this month, Coley announced a $5 million milestone payment from
French partner Aventis Pharmaceuticals regarding a new aerosol treatment
for allergic respiratory diseases such as asthma.
Comments (0)

DNA Fragments Kill Melanoma Cells Posted Friday, September 10, 2004 by arjuna
Finding may lead to new treatments for deadly form of skin cancer

THURSDAY, Sept. 2 (HealthDayNews) -- Certain DNA fragments can destroy melanoma cells, says a Boston University School of Medicine study.

In research with mice, the researchers found that small DNA fragments called T-oligos can cause extensive death in human melanoma cells and that surviving melanoma cells become less aggressive. This finding may help lead to new treatments for melanoma, the most deadly form of skin cancer.

The study appears in the September issue of the FASEB Journal.

"Melanoma is a dreaded disease, resistant to all treatment modalities now available once it has spread beyond the skin. Our results are encouraging and we are very hopeful this finding will provide a novel means of treating melanoma," study leader Dr. Barbara Gilchrist, a professor of dermatology, said in a prepared statement.
The same research team also found that T-oligo fragments delayed and prevented skin cancer in hairless mice exposed to ultraviolet (UV) light. Comments (0)

Shielding Your Skin From the Summer Sun Posted Thursday, August 19, 2004 by arjuna

The truth about wrinkles, skin cancer, sunburns and skin rashes

By Karen Pallarito
HealthDay Reporter

TUESDAY, Aug. 17 (HealthDayNews) -- Americans have a passion for the great outdoors but often seem downright lackadaisical about protecting their skin from the sun's damaging rays.

Myths about sun exposure -- and there are quite a few -- may encourage people's risky behaviors, experts say.

Since the mid-1980s, Americans have been warned that they get about 80 percent of their lifetime dose of damaging ultraviolet (UV) radiation by age 18. It's no surprise, then, that many adults shrug off skin-protection advice; they think that damage has already been done.

But recent studies suggest that warning is false. One study published last year in the journal Photochemistry and Photobiology blames the erroneous message on a mathematical misinterpretation of published data. Americans actually get less than 25 percent of their lifetime UV dose by age 18, investigators from the United States and the Netherlands concluded.

"Sun damage is cumulative throughout your life," explained Linda Rutsch, director of the U.S. Environmental Protection Agency's SunWise educational program, which teaches children and their adult caregivers about protecting themselves from overexposure to the sun.

UV damage from the sun is the major cause of skin cancer. One in five Americans will develop skin cancer in their lifetime, and one dies every hour from the disease, the EPA says.

Cases of melanoma, the most serious form of skin cancer, have doubled in the past two decades and will continue to climb, the agency predicts.

Nonmelamoma skin cancers, while less deadly, can result in serious health problems and disfigurement. The most common types are basal cell carcinoma, which causes the appearance of small, fleshy bumps, and squamous cell carcinoma, which produces nodules or red, scaly patches.

If you're an adult, it's not too late to smooth on sunscreen and don a wide-brimmed hat. "You really do still need to protect yourself," Rutsch insisted.

SunWise's main focus is persuading kids to adopt good sun-safety habits while they are young to avoid skin cancer and other serious sun-related problems later in life.

Appealing to sun-worshiping teens does present a challenge. To get middle schoolers' attention, SunWise uses posters developed by the American Academy of Dermatology that show a baby, a cheerleader, and a buff young man, each with very wrinkled faces. It sends the message that wrinkling is not a fact of aging; up to 90 percent of the visible changes to the skin are caused by sun exposure.

"With these kids, just seeing the wrinkles gets through to them because they care so much about their appearance," Rutsch noted.

Americans' love of the sun can make skin protection a tough sell. A recent report from the American Cancer Society shows many kids are not taking sun protection seriously. Three quarters reported getting sunburns during the summer months.

Like teenagers, many adults are equally clueless about the damage the sun can cause.

"The most common myth -- and I still can't believe it -- is that a little bit of tan protects you from the sun," said Dr. Lynn McKinley-Grant, a private practice dermatologist and spokeswoman for the American Academy of Dermatology (AAD).

"Even though you don't burn you're still getting sun damage," she said.

Excessive sun exposure, especially blistering sunburns incurred during childhood, can promote malignant melanoma, the AAD says. But there's also evidence that UV radiation used in indoor tanning equipment may cause melanoma, too.

A vaccine currently in clinical trials is showing promise for people with advanced cases of melanoma, McKinley-Grant said. At the moment, though, the best hope for patients is to diagnose their cancer early and remove it surgically, before it spreads to other parts of the body, she said.

If premature aging and skin cancer aren't scary enough, here's another reason to take precautions when you're in the sun: Certain medications and medical conditions can react with ultraviolet light, causing people to burn quickly, a phenomenon known as "photosensitivity."

Scores of commonly used drugs can, in some people, cause phototoxic reactions. The list includes antibiotics, such as tetracycline; anti-hypertensive medications, like hydrochlorothiazide; and even common pain relievers, including ibuprofen and naprosyn.

Certain herbal products can cause photosensitivity, too. Bergamot oil, used to flavor Earl Grey tea, is one that has a strong phototoxic effect.

Skin exposure to certain plants along with sunlight also can produce a sunburn-like response. Limes have been implicated in a number of reported cases.

Another kind of photosensitivity, called photoallergy, produces an itchy rash when a person is exposed to sunlight. It is caused by certain medicines and fragrances. Some people even have photoallergic responses to sunscreens containing PABA, a tanning agent.

You can't avoid the sun, but experts recommend taking certain precautions to reduce your risk of premature aging, skin cancer and other sunlight-induced skin reactions.

Since the sun's rays are strongest between 10 a.m. and 4 p.m., it's best to limit exposure during those hours.

"If your going to the beach, take a good umbrella with you," advises McKinley-Grant. "You can wear a good waterproof sunscreen." Just don't sit there and bake.

Before the kids go out, make sure to slather them with sunscreen, too. SunWise's Rutsch recommends using a broad-spectrum sunscreen that protects against both UVA and UVB rays and reapplying it frequently. Look for sunscreens with a Sun Protection Factor (SPF) of at least 15.

Seeking out shade and covering up as much as possible are also simple measures that can save your skin.

"Children, especially, need to be active; we certainly aren't encouraging kids to stay indoors," Rutsch said. "Just try and do as many of the steps as possible."

Comments (6)

Aid Cancer Detection Posted Thursday, August 12, 2004 by arjuna
July 27, 2004

BY LINDA H. LAMB KNIGHT RIDDER NEWSPAPERS

Judy Poarch hadn't noticed anything different about that spot above her knee.

ABOUT MELANOMA

Melanoma, which is diagnosed in about 53,600 Americans each year, is the most serious type of skin cancer.

A 2002 study found melanoma death rates were declining somewhat in younger patients -- who might be getting the message about sunscreen -- but increasing in older men and women.

Close to 8,000 Americans are expected to die from melanoma this year.

Melanoma is 10- to 15-times more common in white people than in black or Hispanic people.

A change in a mole's appearance might be an early sign of melanoma. However, half of melanomas develop in skin that previously appeared normal.

Risk factors include having fair skin, personal or family history of skin cancer, having many moles (more than 50), sun exposure, having at least one severe, blistering sunburn as a child or teenager and a weakened immune system.

Things to watch for in moles: asymmetrical shape (not perfectly round), irregular border, uneven color (may include black, brown, tan, white, gray, red, pink or blue), increase in size.

Prevention: Protect skin by avoiding sun from 10 a.m. to 4 p.m., use sunscreen, cover up, protect eyes with UV ray-absorbing sunglasses and wear a wide-brimmed hat.

On the Web: Melanoma Patients' Information Page is www.mpip.org. The National Cancer Institute site is www.cancer.gov (then search for "melanoma"). "It was just a little bitty freckle on my leg," said Poarch, 56. "I'd had it for years and years."

But when her daughter said she thought the spot was changing, Poarch sensed fear. A cousin had been diagnosed with skin cancer. Poarch looked at the freckle more closely.

"It was a little bit raised and a little bit darker."

She had melanoma, the deadliest of skin malignancies -- accounting for only 4 percent of skin cancers but 79 percent of skin cancer deaths.

"The doctor didn't think it looked cancerous, but then he said, 'Well, we're just going to take that off.' When it came back as melanoma, I was totally in shock. . . . I had 10 million questions."

Tops on her list was how to spot future melanomas. Recently, she embarked on what she hopes will be a solution.

Poarch, a Georgia resident, went to South Carolina to have a MoleMapCD made. The MoleMap is a photographic map of her body that will help her keep track of every mole, scar and freckle.

Developed by James Grichnik, a dermatologist and researcher at Duke University, it involved posing for pictures by a medical photographer who focused on 33 sections of her body. The photos are processed and 33 images are loaded onto two CDs.

Her dermatologist gets one to use for comparison during checkups. Poarch gets the other to use at home. Clicking on a thumbnail photo on her computer screen, she'll get an up-close look at her skin, section by section.

Poarch admitted she had been a little panicky about a recurrence of cancer. She finds the MoleMap concept reassuring.

"You know exactly where the moles are on your body. You know what they look like, and every few months, you can look and see if anything's changing."

When patients such as Poarch face a disease as deadly as melanoma, naturally they're worried about moles that might pop up where the sun doesn't shine.

But as in her case, sun exposure is precisely what causes most melanomas, doctors say.

"Years ago I was out in the sun a lot," Poarch said. "Didn't use sunscreen; didn't think much about it."

Just one severe, blistering sunburn in your youth makes you more likely to develop skin cancer. Melanoma numbers have been stable in recent years, but they've crept up in older Americans. And an indoor tan is no safer than one you get at the beach.

Having a lot of moles is a risk factor and the larger the mole, the greater the risk that melanoma will develop. But melanoma also develops in normal skin. Half of melanoma cases will materialize not in a mole, but in skin that previously looked perfectly normal.

Cost of the MoleMapCD procedure is about $400, which insurance may cover. (Ask your doctor for information, or visit www.digitalderm.com).

Grichnik has been working with the system for about 10 years, trying to make it more user-friendly for doctors and consumers. Melanoma, like less serious skin cancers, usually is curable when found early, according to the American Cancer Society.
Dermatologists using MoleMap say it's most useful for dealing with two

problems: high risk and high anxiety. Those two things can go together, of course. Having just one melanoma can be so nerve-racking that some patients rush to the doctor to have every new freckle surgically removed -- which means more anxiety, expense and scars.

Grichnik followed 526 patients using MoleMapCD for an average of 2.4 years each. Tracking their skin condition with the CD photos, he found that an average of 1.5 skin biopsies were performed per patient, per year. He said that number was significant because previously, the patients had been having an average of six biopsies a year.
Removing every new mole just isn't necessary, Grichnik said. Comments (1)

Human Monoclonal Antibody Helps Fight Advanced Melanoma Posted Tuesday, August 3, 2004 by arjuna
http://www.cancerwise.org/August 2004/
The University of Texas
M.D. Anderson Cancer Center

Early testing of an experimental human monoclonal antibody has shown a striking benefit in patients with advanced melanoma, according to M. D. Anderson researchers.

Tumors disappeared in three of 39 patients who were given a single injection of CP-675,206, a human monoclonal antibody manufactured by Pfizer Inc. Tumors shrank in a fourth patient, and cancer stopped growing in five other patients. These responses have remained since the patients’ initial treatment, which ranged from 13 to 28 months ago.Dr. Luis Camacho Photo

Most of the patients in the clinical trial had advanced melanoma, which has a median survival of less than a year, says the study’s principal investigator, Luis Camacho, M.D., assistant professor in M. D. Anderson’s Department of Melanoma Medical Oncology and a member of the institution’s Phase I Clinical Trials Group.

“We were very pleasantly surprised to find such objective antitumor responses in a Phase I clinical trial, which is designed to find the ideal dose and to look for side effects,” Camacho says. “These results are very early, but they are encouraging to us because there are no good agents available to treat malignant melanoma once it has spread.”

Tolerable side effects

Researchers gradually increased the amount of the initially tested dose by 1,500 fold, evaluating seven different dose levels, before they found higher doses that both produced a response and had tolerable side effects. Most patients who didn’t respond to the drug were those treated with lower doses, the investigators say.

The study was conducted at M. D. Anderson and at the University of California, Los Angeles. A collaborating researcher is Jesus Gomez Navarro, M.D., clinical director of the monoclonal antibody program at Pfizer Inc., which developed the antibody and is sponsoring the clinical trial. The researchers presented their findings at the annual meeting of the American Society of Clinical Oncology in June.

Similar to vaccines, CP-675,206 seems to continue to work long after patients receive the single two- to four-hour injection, Camacho says. “We believe the monoclonal antibody enlists the immune system to fight any new cancer cells trying to grow,” he says.

The antibody may work particularly well in melanoma, he adds, because previous research has shown the immune system, if activated, can recognize this cancer.

Because the antibody allowed the immune system to attack cells that “looked” similar to the body’s own, researchers worried that it could produce autoimmune disorders such as rheumatoid arthritis. But the only side effects observed, including rashes and diarrhea, occurred at the highest doses and were resolved without long-term problems, Camacho says.

Based on the results, Pfizer has launched a Phase II study, which is enrolling 100 patients at seven institutions nationwide. Camacho also serves as the principal investigator for this trial.
For more information about the Phase II multiple-dose CP675,206 study for patients with previously treated metastatic melanoma, call study coordinator Charla Parker, RN, at (713) 745-1042 or data manager Carolina Guitierrez, M.D., at (713) 794-1022. Comments (0)

Cloning experiment shows cancer reversible Posted Monday, August 2, 2004 by arjuna
Last Updated: 2004-08-02 10:34:45 -0400 (Reuters Health)

By Maggie Fox

WASHINGTON (Reuters) - The results of a cloning experiment show that the body may have the ability to reverse cancer, U.S.-based researchers said on Saturday.

They cloned mouse embryos from a melanoma skin cancer cell, and created healthy adult mice using some of the cloned cancer cells, showing that malignancy is not the inevitable fate of a cancer cell.

"This settles a principal biological question," said Dr. Rudolf Jaenisch, of the Whitehead Institute at the Massachusetts Institute of Technology, one of the country's leading experts in cloning.

He said while the genetic elements of cancer cannot be reversed, the epigenetics -- how the genes are actually turned on and off -- can be.

The finding, published in the journal Genes and Development, point to a new way to treat cancer, said Lynda Chin of the Dana-Farber Cancer Institute and Harvard Medical School, who worked on the study.

"Drugs that target the cancer epigenome may prove to be a key therapeutic opportunity for diverse cancers," she said in a statement. In other words, it might be possible to silence a cancer gene.

Cancer begins when certain genes mutate, or when a certain, inherited version of a gene somehow gets turned on.

This can happen through various so-called epigenetic processes -- when other molecules in a cell affect genes without actually altering the sequence of DNA.

In the experiment, Konrad Hochedlinger and Robert Blelloch, both researchers in Jaenisch's lab, took the nucleus from a melanoma cell and injected it into a hollowed-out mouse egg cell.

This started the egg growing as if it had been fertilized by sperm.

They did not allow this embryonic mouse to develop, but harvested from it embryonic stem cells -- immature cells that have the potential to become any cell in the body at all.

They put these stem cells into healthy mouse blastocysts -- very early embryos only a few days old. Some of these developed into healthy, normal mice.

"It's important to note that the stem cells from the cloned melanoma were incorporated into most, if not all, tissues of adult mice, showing that they can develop into normal, healthy cells," Blelloch said. They included skin pigmentation cells, immune cells and connective tissue.

This could only have happened if the cancer cells had lost their malignant properties, at least temporarily, the researchers said.
But when certain cancer-related genes in these mice were activated, they developed malignant tumors at a much faster rate than normal mice, the researchers added. Many researchers want to try similar experiments with human cancer cells, but the administration of President Bush forbids the use of federal funds for such study because it would involve the creation of what is technically a human embryo. Comments (3)

Menace of melanoma Posted Wednesday, July 21, 2004 by arjuna
By Jen Waters THE WASHINGTON TIMES Published July 20, 2004

Henry Lichtenstein of Forestville survived the wrath of Adolf Hitler. Now he is working on defeating skin cancer. During World War II, Mr. Lichtenstein, 82, who is Jewish by heritage, was imprisoned in several concentration camps, including Auschwitz, Mauthausen and Birkenau. Originally from Lodz, Poland, he also suffered in the Lodz ghetto at the hand of the Germans. While under the oppression of the Nazi regime, he was forced to work outdoors in scorching weather, and he suffered several severe sunburns. About 55 years later, Mr. Lichtenstein developed melanoma, a form of skin cancer. The growth on his back was removed surgically in March 1998. He also has developed non-melanoma skin cancers and pre-cancerous tissues that have been excised. "In the concentration camp, you would stay in the sun all day long," he says. "When it got hot, you would take the shirt off. ... Yesterday, I was cutting my grass, and I wore long sleeves, and I have a nice little hat." The number of people developing melanoma is increasing faster than the number for any other form of cancer, according to the National Cancer Institute. In 2003, the American Cancer Society estimates there were 54,200 new cases of melanoma in the United States and about 7,600 deaths. Melanoma accounts for about 4 percent of skin cancer cases but causes about 79 percent of skin cancer deaths. Excessive exposure to sunlight doesn't account for all melanoma, however, says Dr. Gary Peck, director of the Melanoma Center at Washington Hospital Center's Cancer Institute in Northwest. Although medical professionals haven't identified the other causes, Dr. Peck says, doctors are sure they exist. The cancer can occur anyplace there are pigment cells, such as on the genitals, in the anal canal, inside the nose or sinuses and inside the eyeballs. "One patient treated for sinusitis wasn't responding to treatment," Dr. Peck says. "Finally, they did an X-ray and found a tumor, and it was melanoma." Until researchers discover other reasons why people have melanoma, the best way to lower the risk of its occurrence is avoiding too much sun exposure and ultraviolet light, says Dr. Catharine Lisa Kauffman, chief of dermatology at Georgetown University Hospital. If people must be in the sun, she says, they should apply sunscreen with at least 30 SPF before going outdoors and reapply it every two hours, more when perspiring. Further, she says, there is no such thing as a "safe" tanning bed. "Try not to be outside unless you absolutely have to between 10 a.m. and 4 p.m.," she says. "You need to wear a hat, preferably with a 4-inch brim. Wear sunglasses with proper UV protection. ... You need to wear sun-protected clothing. Toss Rit Sun Guard in the wash with clothing to increase its SPF." Factors that increase the risks of melanoma are having more than five serious sunburns as a child, red hair, pale skin, blue or green eyes, freckles, lots of atypical moles, an outdoor occupation, and relatives with melanoma. "To a certain extent, we're a slave to pop culture," Dr. Kauffman says. "If we could get Britney Spears to go pale, we'd be doing great. Nicole Kidman is a good dermatological advertisement." If melanoma is found, patients should return to their doctor for checks every three to six months until the doctor says otherwise, Dr. Peck says. He thoroughly examines Mr. Lichtenstein for new lesions, including on his lips, his scalp, his ears, under his toenails and on the bottom of his feet. The doctor uses a dermascope to examine moles and dark spots on his body. In addition to melanoma, Dr. Peck also searches for other malignant patches, such as basal cell skin cancer and squamous cell skin cancer. "I had one patient where the hairdresser found the tumor," Dr. Peck says. "Sometimes, the part in the hair line can have melanoma; sometimes, under the hair." On other patients, such as Riaz Latifullah, 47, of Northwest, Dr. Peck uses mole mapping, a procedure in which he takes pictures of the skin and magnifies them to analyze skin cancer risk. The images are stored in a computer and are used for comparison during future visits. "I know that melanoma can kill," says Mr. Latifullah, who visits Dr. Peck every six months. "I know that if you catch something that might be cancerous early you can treat it. Given that I have more moles than the average person, it makes sense for me to do it. As a child I ran around in the summer without a shirt on and got very tanned. Now I'm persistent about wearing a wide-brimmed hat." Adults also should make sure to protect their children. Sunburns in the first 10 years of life are the most critical, says Dr. Peck, who has two dozen young patients with melanoma, the youngest of whom is 10. Because there is no known cure for melanoma, early diagnosis is key. Finding a way to thwart the growth of melanoma has been the goal of much of the research funded by the National Cancer Institute in Rockville, says Dr. Scott Saxman, senior investigator in the cancer therapy evaluation program. Recently, scientists have identified a mutation -- a place in the cell where the DNA has changed, often in a bad way -- in one of the signaling pathways referred to as the BRAF gene. A pathway is a mechanism by which cells decide when to grow and divide. Because skin cancer probably has something to do with normal cells undergoing a transformation to malignant cells, finding the mutation has been a significant discovery, Dr. Saxman says. "If we understand better the abnormalities in the cell that have made them a cancer cell, that gives us better information to target the abnormalities," he says. "There is a big emphasis on learning more about the biology of melanoma and how it undergoes the process of being malignant, why it spreads from one space to another, and why it doesn't seem to be sensitive to chemotherapy, like some diseases." More doctors and scientists need to study melanoma and work together effectively, says Bill Marsch, acting executive director of the Melanoma Research Foundation in Princeton, N.J. The organization gives several research grants each year. The association also helps existing melanoma research communities share information through the Society of Melanoma Research, which consists of scientists from around the world. The next meeting will take place in Phoenix in November. "Melanoma has never been attractive to young scientists," he says. "Our goal is to provide grants to encourage young researchers to go into melanoma research." The ABCD Rule for Early Detection of Melanoma Almost everyone has moles. The vast majority of moles are perfectly harmless. A change in a mole's appearance is a sign that you should see your doctor. Here's the simple ABCD rule to help you remember the important signs of melanoma and other skin cancers: A is for ASYMMETRY: One-half of a mole or birthmark does not match the other. B is for BORDER: The edges are irregular, ragged, notched, or blurred. C is for COLOR The color is not the same all over, but may have differing shades of brown or black, sometimes with patches of red, white, or blue. D is for DIAMETER: The area is larger than 6 millimeters (about 1/4 inch -- the size of a pencil eraser) or is growing larger. Other important signs of melanoma include changes in size, shape, or color of a mole or the appearance of a new spot. Some melanomas do not fit the ABCD rule described above, so it is particularly important for you to be aware of changes in skin lesions or a new skin lesion. Other warning signs are: A sore that does not heal A new growth Spread of pigment from the border of a spot to surrounding skin Redness or a new swelling beyond the border Change in sensation ? itchiness, tenderness, or pain Change in the surface of a mole ? scaliness, oozing, bleeding, or the appearance of a bump or nodule.
Source: http//www.fightcancer.org/ACSWW Comments (3)

Why Do Men Get Sunburned? The Problem Lies Between Their Ears Posted Tuesday, June 22, 2004 by arjuna
June 21, 2004
New York Times

By DONNA WILKINSON

M EN over 50 are twice as likely as women to develop skin cancer and, even more sobering, to die from it, according to the American Cancer Society.

Experts say the reason lies not in men's skin -- but in their brains. Hatless, sunscreenless, heedless, men have made fewer changes in the decades of warnings about overexposure to the sun than women have.

"Women get the health message early on," said Dr. Darrell S. Rigel, clinical professor of dermatology at New York University Medical Center. "Under the age of 40, more women than men get skin cancer, but by 80, the ratio is 2 to 1, men to women. Women's skin is more sensitive to sun damage in terms of appearance, so they tend to change their behaviors earlier."

Men are at higher risk because they often have more sun exposure. For instance, they do more outdoor recreation and more outdoor work, as construction workers, longshoremen, fishermen or farmers.

But men are less apt to take precautions. Though susceptible to skin cancer on the face, nose, neck, scalp, ears, chest, back and shoulders, they are not inclined to wear protective clothing like long-sleeved shirts or wide-brimmed hats in the sun. Men like baseball caps, but they do not provide full coverage. "Baseball caps protect only the forehead and face to the tip of the nose," said Dr. Jeffrey Dover, associate clinical professor of dermatology at Yale University School of Medicine. "They provide no protection to the side of the face or neck."

Hats are especially important for men who are bald or losing their hair. "We see a tremendous amount of precancers and squamous cell carcinoma on the scalps of balding men, and a hat is by far the best sunscreen because men are not likely to put sunscreen on their heads," Dr. Dover said.

Not only are men unlikely to put sunscreen on their heads, but they are unlikely to put it on at all. "It's a major ordeal for many of us to shower, shave and brush our teeth," said Dr. David Swanson, assistant professor of dermatology at the Mayo Clinic in Scottsdale, Ariz. "The application of sunscreen adds another layer of self-maintenance and complexity."

Then there's the "goop" factor. "If you ask most men if they like to put cream on their faces, the answer is no, because they don't like the feel," Dr. Dover said.

Men are also less vigilant about checking their skin. A 2001 study by the American Academy of Dermatology found that middle-aged and older men were the least likely to perform self-examinations or visit a dermatologist. Doctors say women are frequently the ones who spot problems. "Often a man will come in and say, `My wife made me come in -- I don't think it's anything,' " Dr. Rigel said, "and it will turn out to be advanced skin cancer."

Though skin cancer is preventable, it is on the rise. The American Cancer Society estimates that more than a million nonmelanoma cancers and 55,100 melanoma cancers will be diagnosed in this country this year. And, the society says, 7,910 Americans will die of melanoma, 5,050 of whom will be men.

The most common types of skin cancer are basal cell carcinoma, which accounts for about 75 percent of all cases; squamous cell carcinoma, accounting for about 20 percent; and melanoma, which is less common but far more deadly, causing 79 percent of skin cancer deaths. There are also precancerous lesions called actinic keratoses, which can become cancerous.

Skin cancer is curable, if detected early. But putting off treatment incurs a high price. "Once a melanoma has spread, basically nothing works," Dr. Rigel said. "A melanoma the size of a dime on your skin has a 50 percent chance of having already spread -- that's why it is so critical to catch it and treat it early."

Prevention is critical because sun damage is cumulative. "With basal cell and squamous cell, it's the chronic sun exposure that does you in," Dr. Rigel said. "But with melanoma, it's the sunburns." Having two or more blistering sunburns in your life can double or triple your chance of melanoma.

How do you know what to look for? Warning signs include new moles or changes in existing moles (irregular pigmentation and borders; assymetrical shape); or sores that do not heal. Also watch for crusting, bleeding, scaling or discoloration.

Ted and Jim Vitas know the importance of prevention. Growing up in a New England beach town, the brothers never thought much about sunscreens when they were lifeguards every summer. "We'd sit all day with our backs to the sun -- we didn't realize it was causing damage," said Ted Vitas, 50. "The only skin care that people talked about then was keeping your skin moist, so we'd put oil on."

During a routine test a few years ago, a nurse noticed an odd-shaped mole on Mr. Vitas's back and urged him to see a doctor. It turned out to be melanoma. And recently, his brother, Jim, 55, was treated for a precancerous lesion found on his back.
Luckily, Mr. Vitas's melanoma was diagnosed as noninvasive. The brothers, who are Dr. Dover's patients, are a lot more sun-cautious. Ted uses a 30 S.P.F. and Jim said he wears "nothing less than a 45." They also go regularly for skin checkups. But Ted still enjoys the outdoors. "You don't have to become a hermit," he said, "but you have to take the appropriate precautions." Comments (2)

For Tans, It's Sprays vs. Rays Posted Sunday, June 13, 2004 by arjuna
New York Times

June 13, 2004


By ALEX KUCZYNSKI

L AST Monday, Sally Blenkey-Tchassova opened the doors to her tiny SoHo salon, Brazil Bronze, and began another day of catering to the beauty demands of New York.

Clients come to her salon, strip naked and stand before her as she mists their bodies with a bronzing solution dispersed through a pressurized air gun (like the kind used to paint cars, just smaller). The 20-minute, $50 treatment transforms the pastiest 98-pound weakling into a buttery-bronze god or goddess.

"It is a fantastic process, isn't it?" Ms. Blenkey-Tchassova said last week, as she sprayed my torso a deep shade of cognac she calls Exotic Dancer. (For clients who prefer a subtler glow, she also offers "WASP Housewife.") "One minute you're white and the next you look like you've spent the week in St.-Tropez."

Ms. Blenkey-Tchassova is just one small part of the $5 billion artificial tanning industry in the United States, but she represents a growing trend. Consumers are increasingly eschewing the classic fake-and-bake approach -- bathing beneath ultraviolet lamps -- and choosing the spray version, in no small part because it avoids the risk of skin cancer.

Advocates of the ultraviolet tan are beginning to feel the heat. The swift growth of the spray-on tan is accompanied by a growing chorus of medical experts who warn of the dangers of ultraviolet tanning.

There is also the prickly matter of impending legislation in California that would forbid anyone younger than 18 from entering a tanning salon without a prescription.

California is already one of 27 states that have passed legislation requiring minors to have permission from a parent or guardian to use tanning beds or booths. No other state has enacted a total ban on teenage tanning such as the California bill proposes, and the ultraviolet tanning industry fears a copycat effect in other states. Customers under the age of 18 make up about 12 percent of tanning clients, according to Today's Image, a trade publication of the tanning industry.

Jeff Nedelman, the spokesman for the Indoor Tanning Association, said that there had been a renewed assault on the industry this year.

The spray-on tan, introduced in a popular form in 2000, has lured customers once wary of tanning salons, salon owners said. The spray-on method is generally endorsed by dermatologists, who have been putting increasing pressure on the ultraviolet tanning industry as tanning salons have attracted teenage clients.

Seeking the burnished toffee shades that popular culture celebrates as a symbol of sexy good health, Americans will make 28 million visits to tanning salons in 2004, Mr. Nedelman said.

The tanning trade group does not break out numbers for how many Americans are visiting salons for spray-on tans versus those going for the old-fashioned fake sunshine variety. According to Looking Fit, another trade publication, more than 2,500 stand-up spray-on units will be in place by the end of the year, a growth of 200 percent over the last four years. (By contrast, there are 25,000 salons in the United States that offer ultraviolet tanning, some with just one bed but others with as many as 30 or more machines.)

Tony Passarello, the chief marketing officer for Palm Beach Tan, a Texas-based chain with 67 salons nationwide, said that the spray-on tan had grown faster than anyone had expected. "It is the single fastest-growing segment for our business in the last two years," he said. Palm Beach Tan salons average 20 to 25 ultraviolet beds, and now many include up to four spray-on booths.

Amy E. Hamaker, executive editor of Today's Image, said that she did not fear for the future of the ultraviolet tanning industry.

"Just like anything else in this world, there's good and there's bad in everything, and moderation is the way to go," Ms. Hamaker said. "It's kind of like eating at McDonald's. A couple of times a week is fine. But if you eat there every day, your chances of getting coronary artery disease go up. However, does that mean you are definitely going to get coronary artery disease? No. In fact, you need a little fat in your diet."

Ultraviolet opponents disagree. "No one should go into a tanning bed," said Dr. Dennis Gross, a New York dermatologist who has studied the relationship between ultraviolet light and skin cancer.

The cause of skin cancer is not debatable, Dr. Gross said. "Ultraviolet light causes skin cancer, period," he said. "Regardless of the source, whether it is natural sun or ultraviolet light bulbs, there is an increased risk of skin cancers, because the effects are cumulative."

In 2002, the Federal Department of Health and Human Services added ultraviolet light to its list of human carcinogens. The Federal Trade Commission, which investigates advertising claims about tanning devices, maintains that long-term exposure to artificial sunlight contributes significantly to premature aging of the skin and to the risk of skin cancer.

Michael Stepp, the president of Wolff System Technology, the country's largest manufacturer of tanning beds and bulbs, said that at any professional tanning salon, technicians should discuss all aspects of tanning and its risks with the potential client.

"In a well-run, professional salon, before you get into a tanning bed, you will have had a discussion about your skin type and what time is appropriate for you," Mr. Stepp said. "They will discuss certain medications that may make you sensitive to UV light. And as a last measure, there are labels on the beds for the consumer, offering guidelines and warnings."

Ultraviolet tanning takes place in tanning beds or booths; clients lie in a coffin-like structure sandwiched by ultraviolet lights (behind plexiglass), or stand in booths that illuminate the tanner from all sides. A base tan requires four to six sessions, and the cost in New York City can vary from $10 to $60 a session.

The spray-on tan is a liquid solution that typically combines aloe vera; a bronzer; and dihydroxyacetone, or DHA, a chemical that interacts with the skin to produce a brown color over several hours, much as the flesh of a cut apple turns brown if left uncovered. Treatments range from $30 for spraying in a stand-up booth, to $150 for a professionally hand-applied tan.

In its efforts to defend against critics in the medical and scientific worlds, the tanning-bed industry has seized upon the work of Dr. Michael F. Holick, a professor of medicine, physiology and biophysics at the Boston University School of Medicine.

Two years ago, Dr. Holick -- who was then also a professor of dermatology -- began to heavily promote research that argued that avoiding sunlight is in itself a health risk, depriving the body of its ability to synthesize vitamin D. Vitamin D insufficiency, Dr. Holick said, may be linked to breast cancer, prostate cancer and Type 1 diabetes. His book, "The UV Advantage," was published last month.

Dr. Holick made clear in an interview last week that he does not promote tanning; he advises people to expose themselves to sunlight daily for a short period (typically, a few minutes, depending on skin type and the time of year). But he has been a regular speaker at Indoor Tanning Association conventions, and the group has used his research as a public relations tool, promoting his research with headlines like "The Holick Safe Sun Health Advice" on its Web site.

The trade group has also awarded Dr. Holick a grant of $50,000 a year for three years to study the effects of sunlight on human health.

"I promote sensible sunlight exposure," Dr. Holick said last week in an interview.

But his colleagues in the dermatology department at the Boston University School of Medicine did not find his approach to be sensible. Dr. Barbara Gilchrest, chairwoman of dermatology at the medical school and chief of dermatology at Boston Medical Center, said Dr. Holick's activities forced her to reconsider his status as a professor.

"Over the years, and in a much more accelerated way in the last six months to a year, Dr. Holick has become the very public poster child for the tanning industry," Dr. Gilchrest said. "I talked to him about the fact that he has a serious conflict of interest with the Indoor Tanning Association that could affect his research. He said he did not believe that." Dr. Holick said last week that he felt no conflict of interest whatsoever, because the $50,000 a year is an unrestricted grant.

"I think people have for far too long been forced to agree with the message that is out there, that is both simple-minded and draconian and putting people at risk, which is `Never be exposed to direct sunlight,' " Dr. Holick said.

At the tanning conventions, past attendees said, Dr. Holick has shown a slide of Gollem, the pale "Lord of the Rings" character, saying, "This is how your dermatologist wants you to look."

When a slide of Darth Vader appears, his comment is: "And this is your dermatologist."

Dr. Gilchrest said that Dr. Holick's work in dermatology "is confusing an issue and encouraging people to do things that are harmful." He resigned from the dermatology department in February.
Certainly, I could have used some vitamin D after my sunless treatment at Brazil Bronze. By Friday, four days after the spray tan, the once startling bronze glow had faded from Exotic Dancer to a patchy pale symphony of whites and browns. It was like watching summer turn to winter in five days, a depressing foreshadowing of the sun's inevitable fade in the fall. Comments (0)

Targeted Therapy Could Be Key to Treatment of Malignant Melanoma Posted Wednesday, June 9, 2004 by arjuna
Medscape Medical News 2004. © 2004 Medscape

Martha Kerr

June 8, 2004 (New Orleans) — A drug that blocks both the pathway for tumor cell proliferation and for angiogenesis in malignant melanoma may finally improve the disease prognosis. Adding it to conventional chemotherapy may result in even greater success, researchers from the University of Pennsylvania in Philadelphia announced here during the 40th annual meeting of the American Society of Clinical Oncology.

Keith T. Flaherty, MD, instructor of medicine at the Abramson Cancer Center of the University of Pennsylvania, presented data on 35 patients with malignant melanoma who received the RAF kinase inhibitor BAY 43-9006, carboplatin (AUC 6), and paclitaxel 225 mg/m2. BAY 43-9006 was given orally in a dose-escalation manner at 100 mg twice daily, 200 mg twice daily, then 400 mg twice daily.

The median age of patients was 47 years. Most were nonresponders to at least one previous trial of chemotherapy.

Carboplatin and paclitaxel were given on day 1 of a 21-day cycle and BAY 43-9006 were given on days 2 through 19. Tumor samples taken previously were assessed to determine the presence of the RAF mutation, and blood samples were taken to assess pharmacokinetics. Patients were treated for at least six weeks.

Dr. Flaherty reported that 14 (40%) of the 35 patients have shown a partial response, and 40% of patients have stable disease. Overall, more than 80% of patients have shown some clinical benefit. Adverse effects were similar to those seen with carboplatin and paclitaxel therapy.

The overall response rate is significantly greater than with chemotherapy alone, Dr. Flaherty said. "Some would argue that there is no standard of care with melanoma," he told Medscape. "But responses rates with carboplatin or paclitaxel are around 15%." He added that there are very few studies using the drugs in combination, but those that have resulted in response rates of around 16% to 17%.

He pointed out that response rate for those who received a second round of chemotherapy after failing a first is extremely low in this patient population, and most of the patients in this study were nonresponders.

Of the 25 tumor samples assessed, 15 tumors (60%) showed the RAF mutation, which is "exactly" the frequency expected in melanoma, Dr. Flaherty said.

"Prospects or patients with malignant melanoma are beginning to change favorably," William W. Li, MD, president and medical director of The Angiogenesis Foundation, told Medscape. The Foundation, located in Cambridge, Massachusetts, is a nonprofit cancer research center. "Targeted therapies are largely responsible for that."

BAY 43-9006 is a multitargeting agent, blocking the vascular endothelial growth factor pathway as well as the RAF pathway, which controls cell growth and proliferation. "BAY 43-9006 is a smart bomb with multiple warheads," Dr. Li explained.

"The goal is to match the drug to the disease," Dr. Li said. Because 60% of patients with malignant melanoma carry the RAF mutation and because it is such a vascular disease, this drug could hold promise for patients with the disease, he speculated.

A major advantage of BAY 43-9006 and many other antiangiogenic agents in development is that they are oral. "We now have the potential of turning cancer into a chronic, manageable disease," Dr. Li said.

The study was funded by Bayer Pharmaceuticals.

ASCO 2004 Annual Meeting: Abstract 7507. Presented June 6, 2004.

Reviewed by Gary D. Vogin, MD
Martha Kerr is a freelance writer for Medscape. Comments (1)

Drugs May Turn Cancer Into Manageable Disease By ANDREW POLLACK Posted Monday, June 7, 2004 by arjuna
June 6, 2004

NEW ORLEANS, June 5 — Brett Smith, the father of two young children, was only 26 three years ago when he was found to have advanced melanoma, a deadly skin cancer. Several drugs failed to stop the cancer, while leaving him frail, depleted and ill.

But two years ago, Mr. Smith began taking an experimental pill along with chemotherapy, and his tumors disappeared. He dropped the chemotherapy nearly a year ago but still takes the pill twice a day. And his disease, though it may return one day, is still at bay.

"No one could take chemotherapy for two years straight; it would just wear you out," said Mr. Smith, a designer for an auto parts company who lives in Cherry Hill, N.J. "But this is simple." The main side effect, he said, is a hoarse voice.

The pill Mr. Smith takes, known by the awkward code name BAY 43-9006, could reach the market in one to three years. It is one of a new generation of "targeted" therapies that are transforming cancer treatment by attacking the underlying molecular mechanisms of the disease.

Some experts see Mr. Smith's experience as a harbinger of a future in which cancer, while not cured, will be held in check for years by drugs tolerable enough to take on a continuing basis.

"Cancer will become a chronic disease that we will manage much the same way we manage high blood pressure or diabetes," said Dr. Andrew C. von Eschenbach, the director of the National Cancer Institute.

Dr. Harold Varmus, president of the Memorial Sloan-Kettering Cancer Center in New York, warns against setting strict timetables that would create "false expectations." But he agreed that it was now a "reasonable goal to dramatically reduce death from cancer, making it a chronic disease."

Targeted therapy is the major theme at the American Society of Clinical Oncology meeting now taking place here. There is a palpable sense of excitement that progress, although limited, is being made against even normally stubborn cancers like those of the lungs and kidneys.

There have already been some heralded successes with these newer cancer drugs. Gleevec, a Novartis drug, has had striking results in chronic myelogenous leukemia and a rare gastric cancer. Avastin, a recently approved drug from Genentech that blocks the flow of blood to tumors, extended lives of colon cancer patients by about five months in a clinical trial.

The enthusiasm has also spread to the pharmaceutical industry, where cancer, once neglected, has become by some measures the most popular disease target. Biotechnology companies in particular view cancer, a disease caused by genes gone awry, as a good match for their techniques of genetic engineering and molecular biology.

Surveys over the last couple of years by the Pharmaceutical Research and Manufacturers of America found 395 drugs in clinical trials for cancer, compared with 122 for heart disease and stroke combined and 176 for neurological disorders. Another survey of only biotechnology-related drugs in clinical trials found nearly half were for cancer, far more than for any other disease.

Indeed, so many cancer drugs are in development that oncologists say it is becoming difficult to run all the clinical trials needed to test them and to determine the best sequences and combinations in which to use them. One session here is titled "Therapy for Metastatic Colorectal Cancer: What Do We Do with So Many Options?"

And when more of these drugs come to market, paying for them could strain the health care system, especially since some of the newer ones cost tens of thousands of dollars for a course of treatment. Bain & Company, the management consulting firm, has estimated that paying for all the cancer drugs likely to come to market would require $60 billion a year, up from $10 billion now.

"The whole U.S. drug market is $150 billion," said Elgar Peerschke, head of the North American health care practice at Bain. "Who's going to pay for that? It's just going to become unaffordable."

Still, there is a long way to go to make cancer a chronic disease. One of the biggest pieces of news at the conference here is that a targeted drug, Tarceva, extended lives of patients with advanced lung cancer. But when the results are announced, the extension is expected to be only a couple of months.

"If I saw a couple more drugs with the impact Gleevec has had I'd be much more excited," said Dr. Otis Brawley, an oncologist and professor at Emory University in Atlanta. "I still think the targeted therapies are the right direction to go, but I think it's important we don't promise the American people something we don't have."

Virtually everyone agrees, too, that any progress will come not only from drugs, but from better means of detecting cancer early, when it is most easily treated, and by preventive steps like getting people to quit smoking.

All cancer therapies are targeted in some sense. Since cancer is characterized by runaway growth of cells, many conventional chemotherapy drugs disrupt cell growth. They also, therefore, attack other fast-growing cells like those in bone marrow and the gastrointestinal tract, leading to such side effects as anemia, infections, nausea and diarrhea.

While chemotherapy has prolonged lives, it is running up against limits. Lung, colon, breast and prostate cancers, the four main killers, essentially "remain incurable by standard chemotherapy" once they have spread to other parts of the body, said Dr. Lawrence N. Shulman, chief medical officer of the Dana-Farber Cancer Institute in Boston.

Targeted therapies attack molecular mechanisms that spur tumor growth, or even cause the cancer. Cancer arises after a series of genetic mutations remove the normal checks on cell growth.

Ideally, targeted therapies would be tailored to the genetic mechanisms responsible for a particular patient's tumor. In the future, scientists say, the genes in tumors will be routinely checked when cancer is diagnosed. And cancers will be classified mainly by their genetic characteristics, not by where in the body they arise or how they look under a microscope.

But knowledge of how to do that is still lacking in most cases. So the drugs are being tried on many patients, but work for only a minority.

Moreover, the targeted therapies are not completely free of side effects. And in some cases, the targeted therapy works best when used with conventional chemotherapy. So toxic chemotherapy is not likely to be eliminated so quickly. The term targeted therapy implies that scientists are rationally targeting the Achilles' heel of cancer. But in truth, in most cases scientists do not really know what the Achilles' heel is, or understand very well the targets they are shooting at.

Tumors grow by multiple mechanisms. So stopping just one of them might not be enough, just as blocking a single road probably would not stop cars from getting to their destinations. Cancer cells also mutate rapidly, so tumors can evolve resistance and neighboring cells in a tumor might be different and not susceptible to the same drug.

"The idea of reforming your tumor cell so it will behave properly, so it's a behaved little guy that you can leave in your body, you just don't want to do that," said Dr. Garth Anderson, a cancer genetics expert at the Roswell Park Cancer Institute in Buffalo. "Over all, if you're trying to cure people with cancer, the way we're curing them now and the way we'll be curing them 10 years from now and the way we'll be curing them 20 years from now is to physically separate them from the tumor by cutting it out with a knife."

Scientists say the mutation problems and complexity might be overcome if targeted drugs are used early, when the tumor cells have not mutated as much. Drugs aiming at different targets might be used together. And the latest trend is to develop drugs that hit more than one target.

The lack of understanding is shown in the case of drugs that block the epidermal growth factor receptor. These include AstraZeneca's Iressa, approved last year for lung cancer, and ImClone Systems' Erbitux, approved in February for colorectal cancer.

The receptor sits on the surface of a cell. When the right growth factor binds to it, it is like a key going into an ignition. It sets off a chain of events inside the cell that leads to cell growth and division.

The receptor is far more abundant on some cancer cells than on healthy cells, so it was thought that blocking the ignition would stem the runaway growth of tumor cells. But it has since been found that there is no clear correlation between the number of receptors on a patient's tumor cells and response to the therapy, suggesting that the premise behind drugs' development was flawed.

"There's a difference between targeting something that's present in the tumor and targeting something that causes the tumor," said Dr. Brian Druker, a professor at Oregon Health and Science University and an important developer of Gleevec.

Only in April did scientists suggest a possible explanation: the relatively few patients who respond very well to Iressa have a genetic mutation that makes their tumors especially dependent on that receptor for growth.

The development of BAY 43-9006, the drug Mr. Smith takes, has also been marked by imperfect knowledge and serendipity. The drug is being developed by Bayer, the German company, and by Onyx Pharmaceuticals, a biotechnology company in Richmond, Calif.

The drug is the first to block a protein called RAF, one of a family of enzymes called kinases that relay signals inside cells.

When certain receptors on the cell surface are activated, the chain reaction of signals that leads to cell growth, with one protein switching on another, is likely to pass through RAF. "One way or the other most cancers turn this pathway on," said Dr. Leonard E. Post, senior vice president for research and development at Onyx.

But at least in kidney cancer, where it has shown most effectiveness so far, BAY 43-9006 might not be working mainly by blocking RAF. Because of "dumb luck," in the words of Dr. Frank McCormick, founder of Onyx and director of the cancer center at the University of California at San Francisco, it turns out that the drug also blocks a protein involved in the flow of blood to the tumor.

Two years ago, in another discovery unforeseen by Bayer and Onyx, scientists in Britain found that RAF was mutated in about 70 percent of melanomas. That immediately raised hopes the drug would be remarkably effective against melanoma.

"We were hoping that the pill, with its relatively mild side effects, would be an overnight sensation," said Dr. Keith Flaherty, an instructor of medicine at the University of Pennsylvania.

But BAY 43-9006 has not worked well against melanoma when used by itself. Dr. Flaherty, however, combined it with chemotherapy and found tumors shrank in 7 of the first 14 patients he treated, including Mr. Smith.

But does the drug work better in the patient with the RAF mutation? That is not yet clear, suggesting full understanding of this target is not yet in hand.

Mr. Smith is not troubled by such questions. "I left the science to them," he said, "and I sit back and enjoy the benefits."
Copyright 2004 The New York Times Company | Comments (1)

Time to Take Precautions to Prevent Skin Cancer Posted Monday, May 31, 2004 by arjuna
May 23, 2004 Sarah Treffinger Plain Dealer Reporter

Debbie Keppler didn't think much of the beauty mark on the side of her head until after it had grown to the size of a silver dollar.

In the 25 years since, the Parma resident has had more than two dozen melanomas removed. She also has made a habit of examining her body for further signs of melanoma, the most serious form of skin cancer.

"It's scary," said Keppler, 52. "People don't understand. They just think, 'Oh, you have a mole. It's like a freckle.' "

Not when it's actually melanoma, which will kill an estimated 7,910 people this year, accord ing to the American Cancer Society's "Cancer Facts & Figures 2004." And more than 1 million new cases of skin cancer will be diagnosed. In addition to melanoma, that number includes diagnoses for the more common cancers of the skin, basal cell and squamous cell carcinomas, which are usually highly curable.

"Skin cancer affects about one in five Americans," said Dr. Marlene Willen, chair of dermatology at MetroHealth Medical Center. "It's definitely an epidemic."

Anyone can develop skin cancer, but some people are more prone to it than others. Risk factors outlined by the American Cancer Society include excessive exposure to ultraviolet (UV) radiation from the sun, fair complexion, family history, multiple or atypical moles and severe sunburns in childhood.

As summer approaches, experts say we can prevent most types of skin cancer by protecting ourselves and limiting our time in the sun.

But for adults, much of the damage is already done. Willen said 80 percent of sun damage occurs by the time we turn 18.

And melanoma is the No. 1 form of cancer in women ages 25 to 29, said Dr. Allison Vidimos, a Cleveland Clinic dermatologist.

"If we teach children early to make a habit of sunscreen use, we're really going to help them," Vidimos said.

Such a habit should include applying sunscreen 30 minutes before going outside and reapplying it every two hours, said Dr. Elma Baron, director of the Skin Study Center at University Hospitals of Cleveland and Case Western Reserve University. She added that it is important not to miss any areas, such as your ears and the middle of your back.

Vidimos said six teaspoons of a "broad-spectrum" sunscreen with a sun protection factor, or SPF, of 15 or higher will usually do the trick.

That breaks down to a teaspoon on your face and neck, a teaspoon on each arm, a teaspoon on each leg and a teaspoon on your back.

Of course, Willen noted, "There is no sunscreen that's a suit of armor." So she tells her patients to cover up.

The American Cancer Society also suggests regular self-examinations to identify skin cancer.

This year's facts and figures publication notes that basal cell and squamous cell carcinomas "often take the form of a pale, waxlike, pearly nodule, or a red, scaly, sharply outlined patch." Meanwhile, melanomas "often start as small, molelike growths that increase in size and change color."

The ABCD rule - A for asymmetry, B for border irregularity, C for color variation and D for diameter greater than 6 millimeters - outlines the warning signs of melanoma, which can quickly metastasize, or spread, to other parts of the body, if not detected early and treated properly.

Vidimos said men and women should look once a month at their skin, including the bottoms of their feet, underarms and scalp, and report to a doctor any changes in the size, shape, texture or color of a mole.

Sometimes, melanoma cases are discovered by a spouse or friend.

Keppler said that's what happened to her daughter, Gemma. During a haircut, a beautician noticed on Gemma's scalp what turned out to be a melanoma. Gemma now sees a dermatologist regularly.

Keppler said she tries to make sure her kids do not sunbathe and doesn't allow them to sit by their pool without the shade of two huge umbrellas.

She has every reason to be vigilant.

Her husband, Wayne, had melanoma that metastasized. He died of bone cancer in 1998.

To reach this Plain Dealer reporter:

streffinger@plaind.com, 216-999-3906
© 2004 The Plain Dealer. Comments (0)

My Turn: That Little Freckle Could Be a Time Bomb Posted Tuesday, May 25, 2004 by arjuna
It took four cancer scares for me to realize that skin care is more than covering my face when I sunbathe Freaky freckles: Regular check-ups saved Susan T. Lennon from potentially fatal skin cancer By Susan T. Lennon Newsweek

May 24 issue - Perched on the edge of the examination table, I was chattering away to my dermatologist, Dr. Penny Lowenstein, as she examined my skin last December. Uncharacteristically quiet, she pulled out a magnifier to peer at my face. "Feel anything strange above your lip?" she asked. My heart sank. Squeezing my eyes shut, I whispered, "No." My palms started to sweat when she said, "Precancerous." It was actinic keratosis, and the treatment wasn't pretty. I had to smear chemotherapy cream over the dime-size spot for the next 12 days—destroying the diseased skin, but turning it into a mass of angry red pustules along the way.

I've been through this skin-cancer thing before. A few years ago I had a basal-cell tumor. Known as "the cancer to get if you've got to have cancer," it's slow growing and it rarely spreads. That was the good news. The bad news was that it was on my forehead. Vanity took flight when I learned that, untreated, it would worm its way into my brain. A plastic surgeon dug it out, leaving me with a perpetually uplifted eyebrow.

I knew that early sunburns trigger skin cancer. When I was a kid, no one used sunscreen. I blistered from burns every summer; no one ever thought twice about it. As a teenager, I slathered myself in baby oil and roasted myself red as soon as the weather warmed. But the only concession I made after my basal-cell diagnosis was to cover my face as I sunbathed in secret. And to go for my yearly skin check.

The next year I was in for a shock. Suspicious spots were cut out and sent to a lab; a few days later I learned that I'd sprouted a dysplastic nevus—a mole that might morph into melanoma—on myneck, a squamous-cell cancer on my collarbone and a melanoma on my shoulder.

Squamous-cell carcinoma is several notches higher than basal on the Scary Cancer Scale. It grows more quickly and more deeply, and pieces can break off and lodge in inconvenient places like your lungs or liver. It seemed impossible that the skin tag on my collarbone, a teeny little bump, could have turned so monstrous.

Melanoma is the most menacing of the skin cancers. Masquerading as a freckle, it can wreak havoc without any symptoms. If it's not caught early, major organs can become riddled with the disease. It's a cancer that usually strikes people in the prime of their lives, and the five-year advanced-melanoma survival rate is grim.

Which is why I was distressed at this latest development. After umpteen precancerous moles, heaps of biopsies and four skin cancers, I scrutinize my skin like a zealot, poring over my pores, inspecting my insteps and even looking "down there." I figured that between my own vigilance and the now quarterly dermatologist visits, I was covered. I was even blase.

But when Dr. Lowenstein handed me a mirror and shone a bright light onto my face, I could barely make out three scaly spots. What I thought was a touch of dry skin was actually a time bomb.

When I told my husband, he blanched. "I can't believe it. Come into the light and let me look." Little did I know that he, too, analyzes my skin relentlessly. "So if you weren't doing these skin checks, this little thing could have killed you?"

Yup. It shook me out of my complacency. Searching the Internet for information on actinic keratosis, I found page after page on skin cancer. And I remembered how disfiguring the treatment for basal- and squamous-cell cancer was—I have enough surgery scars to call myself the Bride of Frankenstein.

Then I stumbled across the Melanoma Patients' Information Page. The "guest book" is chilling. A pregnant mom's 38-year-old husband has end-stage melanoma. A woman with three young children agonizes over two nasty therapies. Someone else writes about her own mom, 58—diagnosed in April, dead the following March.

Though teens obsessed with tanning beds have become enough of a trend to be dubbed "tanorexics," many more kids avoid skin cancer now because of prevention efforts. What about the rest of us? We know we should stay out of the sun—and I've kicked my sunbathing habit—but what about all the years we didn't? The damage is done, but we can do something about it.
Got an irregular-shaped brownish-blackish spot, or what looks like a zit but lingers and bleeds, or an itchy bump that seems a bit bigger this month? Call a skin specialist, and have yourself checked from head to toe. Catch a cancer early and you might avoid mutilating operations, brutal treatments and early death. Not quite five years after my melanoma, I'm alive today thanks to skin self-checks and an astute dermatologist. Smaller than a pencil eraser, that freckle wanna-be could have erased my whole life. Lennon lives in Rocky Hill, Conn. © 2004 Newsweek, Inc. Comments (4)

A KILLER TAN Posted Saturday, April 17, 2004 by arjuna
Prevention magazine, May 2004

A Killer Tan Burning issue: Are UV rays in tanning beds really safe?

by Hallie Levine

Michele Hoard has stayed away from tanning beds and out of the sun since she was diagnosed with malignant melanoma, a deadly form of skin cancer, in January 2003. But when she heard that a tanning salon near her home in Minneapolis was offering a sunless, spray-on self-tanner, she decided that it was worth finding out more about the tanning alternative.

"I walked in and asked the guy at the front desk about it, and he recommended instead that I go into one of the tanning beds for 10 minutes before trying the spray," recalls Hoard, 35. "I said, I can't tan; I'm a melanoma survivor.'"

His response floored her.

"He just waved his hand and said, 'No worries--the tanning beds are good for you because they contain mostly UVA rays, which reduce your risk of cancer.' I couldn't believe he was advocating tanning to someone who'd had skin cancer."

Lisa Whitehead, now 42, bought an indoor-tanning membership and started going every other day because "the manager told me that the beds were FDA-approved and that the indoor rays were safer than the sun because all the bad, cancer-causing agents were filtered out," she says. Four years later, she noticed a black spot on her upper arm and decided it had to be a beauty mark. "I didn't really think about it until a few months later, when I went to see my dermatologist and she told me I needed to have it biopsied," Whitehead recalls. Two days later, she learned that she had stage 1 melanoma--at age 27. "I went back into the tanning salon and screamed at them," says Whitehead, now married with two children. "I told them that they had lied and that their beds had given me cancer."

Hoard and Whitehead are not alone. In an investigation into the $5 billion tanning salon industry, Prevention has found that hard-sell tactics and false assurances of safety are luring women into putting themselves at risk for cancer, disfigurement, and worse. Not only do some industry representatives claim that tanning is safe; they also insist that soaking up ultraviolet radiation from sunlamps is actually good for you. Read on for what you must know to protect yourself--or your teenage daughter--from this dangerous misinformation.

Booming Business There's no doubt that the tanning business is booming. Sales figures for Hollywood Tans, the largest tanning salon chain in the country, have surged more than 450% since 2000, and industry numbers are up overall: 29 million people visited a tanning salon in 2003, compared with 27 million in 2000, reports the National Tanning
Training Institute, an industry education group based in Phoenix. The group claims that of the 1 million-plus people who spend time and money in tanning salons each day, 70% are women, and 53% are between the ages of 20 and 39. And, reports the industry, the two fastest-growing categories of indoor-tanning-bed users are female teens between 16 and 19 and women between 40 and 49.

What may be drawing them, in part, are the tanning industry's unprecedented and aggressive new marketing tactics, which have confused consumers about the real risks of tanning beds. These started last fall, on the heels of a 2-day October summit in Washington, DC, where public health officials from the National Institutes of Health (NIH) reviewed evidence suggesting that certain groups of Americans don't get enough vitamin D in their diets. As remedies, experts recommended supplements, vitamin-fortified dairy products, and brief exposure to sunlight, because UV radiation helps the body manufacture vitamin D.

Indoor-tanning businesses took that baton and ran with it, boldly offering their services as a solution to what they've dubbed "a life-threatening epidemic of vitamin D deficiency."

"My wife uses tanning beds because she's concerned about vitamin D deficiency," says Michael Stepp, CEO of Wolff System Technologies, a major manufacturer of tanning lamps in Marietta, GA. "Sure, she's Norwegian with a lot of moles, but she knows that the health benefits of a small amount of sun exposure far outweigh the risks."

Such carefully crafted messages and testimonials extolling the benefits of tanning "are convincing women that tanning salons are safe," says Mark Naylor, MD, a dermatologist at the Oklahoma Medical Research Foundation, an independent biomedical research organization in Oklahoma City. The industry spin also has dermatologists scrambling to head off
the public's misplaced concerns regarding the need for vitamin D. "These claims are ludicrous," says James Spencer, MD, professor of dermatology at New York's Mount Sinai School of Medicine and a spokesman for the American Academy of Dermatology. "The great majority of Americans get adequate amounts of vitamin D." In addition, the amount of sunlight a fair-skinned person needs to make a whole month's supply of vitamin D is about 5 to 10 minutes three times a week--just on the face. "The same UVB rays that create vitamin D can destroy it in your skin," warns Robert Heaney, MD, John A. Creighton professor of medicine at Creighton University and a speaker at the NIH conference last fall. So with UVB, more exposure isn't better--even for synthesizing vitamin D. Indoor-tanning packages, however, are often sold in monthly units of unlimited tanning.

Tanning and Cancer Murky science and controversial claims are nothing new for the indoor-tanning industry, which used to advertise its tanning devices as safer than the sun. Now, it employs marketing practices that are even more aggressive than the tobacco industry's methods prior to the antismoking backlash of the 1970s. "When the first research came out showing that smoking was dangerous, the tobacco industry's response was always, 'We don't know. There's just not enough science,'" says Spencer. "But here, the tanning industry is not just saying it's not dangerous; it's saying tanning is actually good for you. The tobacco industry never said that, to my recollection."

Even more worrisome than the tanning camp's assertions regarding vitamin D is its position on cancer, which it says can be caused by sun deprivation and prevented by tanning lamps. The claims--that brief exposure to tanning devices can ward off cancers of the colon, prostate, and breast, as well as a host of other debilitating diseases,including osteoporosis, arthritis, and depression--do contain a tiny
kernel of truth. They're based on research conducted largely by Michael Holick, MD, director of the Vitamin D, Skin, and Bone Research Laboratory at Boston University, with partial funding from the tanning industry. But Holick concedes that the amount of sunshine you need is minimal, "and you don't need to go to tanning salons to get it."

Other experts are even more skeptical, pointing out that scientific evidence suggests only that vitamin D may help protect against colon cancer. "Even there, we're not sure if it's due to the vitamin alone or in combination with calcium," says dermatologist Martin Weinstock, MD, PhD, chair of the American Cancer Society's Skin Advisory Group.

The tanning industry's other major point--that avoiding the sun (or sunlamps) may put you at increased risk of prostate, lung, breast, colon, ovarian, and pancreatic cancers--is based on research conducted by William Grant, PhD, a NASA scientist whose work is partially funded by the Indoor Tanning Association. These claims, detailed in an October
2003 industry press release, have been dismissed by the dermatology community. "It is dangerous to mislead the public into thinking sunlight is a safe and effective 'cure' for other health conditions," says Raymond L. Cornelison Jr., MD, president of the American Academy of Dermatology.

For all the urgency the tanning salon industry places on cancer prevention and health, the one disease it downplays is skin cancer--especially melanoma.

"One of the more common beliefs offered as 'fact' by some members of the medical community and people opposed to tanning is the idea that natural or artificial sunlight can trigger melanoma," says Wolff System's Stepp. "The truth is, melanoma is believed to be genetically triggered." Weinstock vehemently disagrees, noting that although "genetic background plays a role, the biggest factor in melanoma is UV exposure." What's more, scientific evidence supports a link between tanning-bed use and skin cancer. A review study published last October in the Journal of the National Cancer Institute strengthened the evidence that tanning beds are helping drive up rates of melanoma, a cancer that kills one American every hour. (The lifetime risk of developing invasive melanoma has increased a whopping 2,000% since
1930.) The JNCI review noted that indoor tanning can increase a fair-skinned individual's risk of developing melanoma by 55%. And it can take a mere 10 indoor-tanning sessions to cause precancerous DNA damage, reports a recent review study by a Kings College London researcher.

Indoor tanning contributes to nonmelanoma skin cancers as well. A 2002 study in the JNCI found that tanning-bed enthusiasts have up to 2 1/2 times the risk of squamous cell carcinoma and 1 1/2 times the risk of basal cell carcinoma compared with nonusers.

Naylor, the Oklahoma dermatologist, has no doubt that indoor tanning is responsible for many new cases of skin cancer. "In the past few years, I've seen an increase in the number of tanning-bed users with skin cancers on parts of their bodies that don't get exposed to sunlight, such as their breasts and buttocks," he says. Kristi Hiltz, 24, of
Baltimore, tanned topless 5 days a week for 4 years but stopped in 1999 when her dermatologist diagnosed melanoma in a mole on her left breast. "My doctor is convinced that my cancer is from indoor tanning, since the spot was always covered by a bikini top whenever I was outdoors," Hiltz says.

Questionable Assurances That UVB and UVA radiation--whether from tanning bulbs or sunlight--can cause skin damage that can lead to cancer is as close to a hard-and-fast medical certainty as science can offer. Yet when Prevention sent a reporter to a tanning salon in the New York area with a question about skin cancer, the sales representative downplayed any link. When the reporter asked the rep what she should do if she had had a squamous cell carcinoma removed from her back, the rep handed her a tube of zinc oxide and said, "If you're worried, just put this on; it'll block any suspicious areas." Medical experts counter that if you've had one squamous cell carcinoma, you're at increased risk for others anywhere on your body--for the rest of your life. At a different tanning salon, a salesperson told our
reporter that squamous cell carcinoma had nothing to do with prior sun exposure. "Not true," says Rex Amonette, MD, past president of the American Dermatological Association and clinical professor of dermatology at the University of Tennessee in Memphis. "We know for sure that exposure to UV light contributes to all types of skin cancer."

Here are two more tanning-industry claims and the facts behind them:

Unlike the sun, tanning bulbs don't burn your skin. The industry did dial down the rays in the 1980s, after it was revealed that the first tanning beds, which emitted mostly UVB light, could cause serious burns and eye damage after less than 1 minute of exposure. In response, many tanning-bed manufacturers greatly reduced the amount of UVB light. That proved not as efficient at tanning, so they developed beds that contain about 94% UVA and 6% UVB rays--about the same ratio as what's in sunlight. The one crucial difference: Studies show that UVA energy levels in tanning beds are up to 15 times stronger than the sun's UVA
rays--and therefore increase the risk of burning.

A "base tan" protects you against sunburn Not likely. A 2002 study from the Technical University, Munich, Germany, found that tanning for at least 6 weeks in UVA beds did not offer any more UV protection than not tanning at all. Shannon Carlino, 32, of Bear, DE, learned the hard way what mounting evidence suggests: Tanning salon tans are probably useless for protecting you against future sun damage. Five years ago, she went to tanning salons three times a week for 2 months because--ironically--she didn't want to burn on her Cancun honeymoon. The move backfired. "I was so fried that I looked like I had raccoon eyes and had to cover them with makeup in all my wedding photos," says Carlino, who was diagnosed with a melanoma on her lower leg in August 2003.

Still, the flattering effects of deeply bronzed skin make tanning-bed use very tempting for millions of women like Melanie Mahaffey, a 23-year-old publicist in Houston who's been tanning indoors twice a week since age 15. "My mom, who also tans all the time, had a small skin cancer taken off her arm last year, so sometimes I worry. But I figure I'm still so young that my skin will automatically rejuvenate
itself," she says. Not so, say dermatologists, who warn that the aging effects of tanning beds are irreversible and that indoor tanning ages skin faster than the sun because of the concentrated levels of UVA."People wrinkle a lot faster from UVA light because it penetrates more deeply and thins out skin's collagen, thus thinning out skin," says Bruce Katz, MD, director of the JUVA Skin and Laser Center in New York
City. "When I see patients, I can tell right away if they've been to a tanning parlor; they've got this crepey look to their skin like they've baked in the sun all their lives. They will look old before their time."

Limited Government Protection When asked about the industry's claims and assurances, Dan Humiston, president of the Indoor Tanning Association, replied that tanning beds are perfectly safe because the government regulates them. "The FDA has strict guidelines on equipment and on maximum exposure time in each bed, and we follow them," he says.
Indeed, the FDA does regulate the amount of UV light that tanning lamps can emit. It also requires that each user wear goggles and that tanning beds carry a warning label stating that UV light may cause skin cancer. However, on visits to several tanning salons, Prevention found that many of these warnings are on top of the machines and thus out of view.
Nonetheless, say salon owners such as David Kim, whose Hollywood Tans franchise is in New York City, if customers get burned, it's because they stay in the beds too long.

At best, consumers are getting mixed messages about the dangers of indoor tanning. Who will help keep them from becoming future cancer victims? The American Academy of Dermatology opposes indoor tanning and supports a ban on the production and sale of indoor-tanning equipment for nonmedical purposes. But "as much as we don't like to admit it, doctors are losing the battle with our public anti-tanning messages," says Amonette. So far, federal agencies seem concerned only in principle with the tanning industry's false claims and have no plans to step up regulation. "Our role is to prevent burns to the skin and
eyes," says Howard Cyr, MD, PhD, chief of radiation biology at the FDA. "We regulate warning labels on the machines. We don't have the resources to inspect 25,000 salons, so we only crack down on tanning salons if we've had a complaint. We don't have any jurisdiction over claims the tanning salons may make."

The Federal Trade Commission, which has jurisdiction over these claims, says it's been a number of years since the tanning industry has been the target of an investigation. "In 1998, the FTC took action against tanning-bed manufacturers for falsely claiming that indoor tanning did
not pose skin cancer and other risks," says Mamie Kresses, a senior attorney in advertising practices at the FTC. When Prevention filled her in on the industry's new pro-health campaign, she told us that the agency is particularly concerned with health-related claims and asked us to send more information.

Meanwhile, women who've been burned by tanning salons are furious enough to go public in the hope that their experiences will serve as a warning to others. Roxanne Smith, 44, of Hanover, PA, stopped using tanning salons in 1999 after a severe burn on her back and buttocks made sitting painful. Then she learned she had melanoma on her lower back. "I know why women go to tanning salons. You go in there and you're lulled into this false sense of security," she says. "The salons say, 'Don't worry, you're safe, you won't burn,' even as they get you to sign a release absolving them of all responsibility. Well, I've had
four biopsies and 12 moles removed since I was diagnosed with melanoma in 2002. My 4 years of tanning in a salon mean a lifetime of disfigurement for me."

The ABCs of UV Rays:

UVA: Relatively weak but long rays that penetrate deep into the skin. Considered a contributing factor in skin aging, wrinkling, brown spots, and blotching. Both the sun and sunlamps contain a mixture of UVA and UVB.

UVB: Shorter, more intense rays that cause burning, tanning, damage, and skin cancer.

UVC: Superintense rays that you don't have to worry about because they are absorbed by the earth's atmosphere and aren't used in sunlamps.

WHAT'S YOUR REAL TANNING RISK? Some skin types burn more easily than others when exposed to UV rays from the sun or tanning lamps. Skin burns are a sign of cell damage that can lead to premature aging and cancer. If your skin type is 1, 2, or 3, dermatologists say you should never attempt to tan.

1. Porcelain (pale skin) Always burns within minutes of UV exposure; never tans

2. White Burns easily; tans minimally

3. Medium white Burns moderately; tans gradually to a light brown

4. Beige or lightly tanned Burns minimally; tans easily to a moderate brown

5. Moderate brown or tanned Rarely burns; tans to a dark brown

6. Dark brown or black Never burns; deeply pigmented

Source
American Academy of Dermatology Comments (0)

Skin cancer a "time bomb," scientists warn Britons Posted Wednesday, March 31, 2004 by arjuna
Last Updated: 2004-03-30 9:44:20 -0400 (Reuters Health)

By Patricia Reaney

LONDON (Reuters) - Skin cancer is a potential time bomb for young
Britons, researchers said on Tuesday.

Despite a 24 percent rise in the last five years in cases of melanoma,
the deadliest type skin cancer, most young Britons are ignoring warnings
about sunbathing.

"Seventy percent of young people are still seeking a tan when they go on
holiday," Dr Charlotte Proby, a dermatologist at the charity Cancer
Research UK, told a news conference.

Young skin is particularly vulnerable to the sun's ultraviolet
radiation, which causes skin cancer, but teenagers and adults are not
taking precautions, according to a new survey.

"Unless young people change their habits and learn to protect themselves
properly in the sun we could be heading for a skin cancer time bomb,"
Proby said.

The poll of 1,800 people commissioned by Cancer Research UK revealed
young women are most likely to sunbathe on holiday and more prone to use
low protection sun screens.

Less than 10 percent of people questioned listed checking for changes in
moles and not burning in the sun as preventive measures against the
disease.

Skin cancer is already the third most common form of cancer in 15-24
year olds in Britain after Hodgkin's disease and testicular cancer and
is the fasting increasing of all cancers.

Malignant melanoma is the most serious type of skin cancer. It accounts
for roughly 10 percent of reported cases of the illness and can spread
rapidly throughout the body, forming secondary tumours.

Almost 7,000 people in Britain were diagnosed with the disease in 2000
and about 1,700 died. It now kills more people in Britain each year than
in Australia, which has a warmer, sunnier climate.

But Proby said more people are fleeing Britain's unpredictable weather
and taking holidays in Spain, Greece, Portugal and other sunny countries.

Since 1971, the number of Britons holidaying abroad has risen from 4,200
to 27,336 in 1994. A large proportion of new cases of skin cancer is
among 15-39 year olds.

"Skin cancer is a major public health issue and we need to come together
as a society to tackle it," said health minister John Hutton, who
announced a 400,000 pound ($727,000) government increase in funding for
a national campaign to raise awareness about the disease.

Proby advised people to avoid the midday sun, to wear T-shirts, hats and
sunglasses and to use a sunscreen with an SPF (sun protection factor) of
at least 15.

She also said people should never let themselves burn in the sun and
advised parents to protect their children.

"Childhood is the most dangerous time to receive a sunburn," Proby added.
Comments (0)

Sun's effects surface with skin cancer Posted Saturday, March 20, 2004 by arjuna
Published in the Asbury Park Press 3/19/04

Toms River dermatologist urges people to have strange spots checked

By MARGARET F. BONAFIDE
STAFF WRITER

TOMS RIVER -- Waiting too long to check on a changing mole may have been
a serious mistake for a former sun enthusiast whose melanoma spread before he sought treatment.


PETER ACKERMAN photo

Everett McAllister (right), with his fiance, Alison DiGiorgio, and his
9-year-old daughter, Danielle, is being treated for melanoma, which has spread to his lymph nodes.

Everett McAllister, 43, of Red Bank Avenue in the Bayville section of Berkeley said he waited more than a year to see a doctor after the mole on his neck began changing colors. By the time he had surgery to remove
it, cancer had spread to his lymph nodes, which also were surgically
removed. Now, doctors are trying to determine the best way to continue
treating him.

McAllister worked outdoors installing fences and doing power washing.

"This is from the sun," he said. "The doctor said it could be from a
sunburn from 20 years ago."

McAllister's "small mole" had darkened to blackish in color. It began
itching a year before he went to see Dr. Rami Geffner at Accredited
Dermatology in Toms River.

Now, two operations later, McAllister, a volunteer firefighter for the
past 10 years, researches on the Internet for information on cancer
treatments while he worries that the disease may come back.

At Accredited Dermatology, office manager Jerry Schlitzer is a busy man
managing the patients who visit the staff at all 12 locations of
Accredited Dermatology, among them several in Ocean and Monmouth
counties. Geffner's partner in business is his wife, Dr. Patricia Tager,
also a dermatologist.

"Everybody is a product of the '60s, and it catches up to you,"
Schlitzer said of people who spend a lot of time in the sun.

Yesterday, Geffner removed a growth from the nose of Janet
Shallcross-Siecke, 68, of the Lanoka Harbor section of Lacey. As a
child, Shallcross-Siecke's family spent summers in the sun. She has
basal cell carcinoma and had surgery yesterday.

"Back when I was young, they said the sun was good for you,"
Shallcross-Siecke said. "It was a good source for vitamin D."

There are other members of her family who have the same type of skin cancer.

"If you have something (on your skin), and it's not healing, get it
checked," she said. "Don't wait."

On Lucille Peters' left cheek is a small patch of irregular shaped
discoloration.

Peters, also of Lacey, had basal cell cancer removed from her cheek
yesterday. She has been a patient of Geffner for the past 15 years.

Geffner used a circular incision around the growth, called the "Mohs"
procedure, to remove the suspected cancerous material. He cauterized the
blood vessels to minimize the bleeding.

"If you catch melanoma early, there is a 100 percent cure rate," Geffner
said.

Skin cancer "can look like a blemish on the skin," he said.


TIM MC CARTHY photo

Everett McAllister's dermatologist, Dr. Rami Geffner of Accredited
Dermatology in Toms River, cauterizes Patrice Cloos' incision after
removing a cancerous growth.

If the suspect mark is bigger than the thickness of about 10 pieces of
paper, the rate at which the cancer cells can grow is much faster, he said.

There are three types of skin cancer, Basal cell carcinoma, Squamous
cell carcinoma and and malignant melanoma. Basal cell carcinoma is most
common. It grows slowly and rarely spreads.

"Basal cell won't kill you," Geffner said.

Squamous cell carcinoma, which growns slowly, can be fatal if left
untreated.

Patrice Cloos, 43, of Toms River had a mole near the base of her left
ear and went to see the doctor. Her mother had metastatic cancer and
died several years ago. Cloos, of Irish descent, is a fair-skinned
blonde who vacationed at the Jersey Shore as a child.

"We would suck up as much sun as we could," she said of her
sun-worshipping days.

Her mole became noticeable on March 7, and she went to her primary
doctor, who refered her to Geffner's office. The bump was removed and
found to be cancerous, and within two weeks, the growth returned.
Geffner removed it again yesterday.

Cloos worries about her 15-year-old daughter's desire to lie in the sun
or its artificial equivalent, the tanning bed.

Geffner said the need to be tanned is causing patients to come in younger.

People with a history of skin cancer in their family are predisposed,
Geffner said. He has one 8-year-old patient with a precancerous growth.

Larry Wager, 83, of Whiting in Manchester has had several cancerous
growths removed from his legs by Geffner. He also blames the sun.

"I spent many years on Jones Beach (Long Island) when I was young,"
Wager said.

For Angel Morrison, Geffner's head surgical nursing supervisor, working
in the busy office is a pleasure.

"I was born to do this," she said of caring for patients. "It is my
calling."

Morrison works with all the doctors in the practice including Dr.
Prabhas Trivedi, a dermatologist. Trivedi remembers McAllister's diagnosis.

"We want to tell patients to come in early as possible," Trivedi said.
Breaking bad news to patients such as McAllister requires "compassion
and some hand-holding. We need to get them to the next surgery as soon
as possible. Most of all, they cannot delay."
Comments (98)

FDA Approves Cancer Fighting Drug Posted Friday, February 27, 2004 by ctustis
Colon Cancer Treatment Not a Cure, Agency Warns
Associated Press
Thursday, February 26, 2004; 6:34 PM

The first drug that promises to attack cancer by choking off its blood
supply won federal approval Thursday, a treatment for advanced colon
cancer called Avastin.

It's not a cure, cautioned the Food and Drug Administration: Avastin can
extend patients' lives by a median of five months, meaning half do
better and half worse.

But it's a significant development. Few other drugs for advanced stages
of this cancer have provided even that much benefit.

Also important, Avastin becomes the first drug proved to work according
to a novel theory that tumors must form a network of blood vessels to
survive -- a process called angiogenesis -- and that shutting down that
process could fight cancer in a completely new way.

Avastin's approval marks "a milestone in a new form of cancer therapy,"
said Dr. Judah Folkman of the Harvard-affiliated Children's Hospital of
Boston, who pioneered the anti-angiogenesis theory 30 years ago.

Manufacturer Genentech Inc. "is to be congratulated for elegant
scientific work that has converted a theory into a therapy," Folkman said.

It was a long, hard road. Folkman made front-page news in 1998 with
reports that his anti-angiogenesis drugs had cured mice of cancer. But
early attempts to make such drugs work in people kept failing.

That may be because doctors initially tested them in the most difficult
of patients, those who had failed numerous chemotherapies, said Dr.
Louis Fehrenbeacher, head of Kaiser Permanente's cancer study program
who helped test Avastin. Tumors that survive repeated treatment seem to
be the hardiest, and anti-angiogenesis will do its best work earlier in
the disease, he said.

Indeed, Avastin is approved as a first-line treatment for metastatic
colon cancer, where the cancer has just spread throughout the body.

In a study of 800 people, half received intravenous Avastin in addition
to routine chemotherapy every two weeks. Not only was tumor growth
delayed in the Avastin patients, but they lived a median of 20 months,
five months longer than those getting standard treatment.

That's a 30 percent increase in survival, which is very exciting, said
FDA Commissioner Mark McClellan.

Some patients did better. Fehrenbeacher points to some of his who have
lived almost three years.

Avastin is a monoclonal antibody, a substance that seeks out and binds
to one of the more than 20 chemicals known to help tumors' blood vessels
grow. The one Avastin targets is called vascular endothelial growth
factor, or VEGF. When Avastin binds to it, VEGF can't stimulate blood
vessel growth, thus keeping tumors from growing by denying them
nourishing blood.

Genentech said it will begin shipping Avastin in three days. The
wholesale cost will be $4,400 per month; in the study, most patients
underwent 10 months of Avastin therapy.

FDA's decision marks the second new treatment approved for advanced
colorectal cancer in as many weeks. Erbitux, the drug at the center of
the stock-trading scandal that brought Martha Stewart to trial, works in
a different way, by blocking growth of the colon tumor itself, not its
blood supply. FDA is allowing it to sell based on studies proving tumor
shrinkage; no one yet knows whether Erbitux will actually help patients
live longer.

Scientists are working to see if Avastin can treat other cancers, too.
It failed as a last-ditch breast cancer treatment, but studies are under
way to see if it helps in earlier stages of that disease and lung
cancer, Fehrenbeacher said.

In all, 30 anti-angiogenesis drugs now are being tested in people around
the world, Folkman said -- including one he developed, called
endostatin, that is showing promising results in a handful of patients
with some rare cancers.

As for Avastin, the FDA cautioned that it occasionally causes some
serious side effects including holes in the colon, impaired wound
healing and internal bleeding.

More common side effects are high blood pressure, fatigue, blood clots,
diarrhea, appetite loss and increased risk of infection because of
decreased white blood cells.

In trading on the New York Stock Exchange, Genentech shares closed at
$103.10, up $7.02, or 7.3 percent.

Comments (0)

Rutgers University Researcher Discovers Gene That Causes Melanoma Posted Monday, April 21, 2003 by ctustis
Mon Apr 21 12:29:22 2003 Pacific Time
Rutgers University Researcher Discovers Gene That Causes
Melanoma; Results Published in Nature Genetics

NEW BRUNSWICK, N.J., April 21 (AScribe Newswire) -- Rutgers
University Associate Professor Suzie Chen has discovered a gene
responsible for melanoma, the most aggressive form of malignant skin
cancer. A paper describing the research by Chen and her colleagues at
the National Human Genome Research Institute will be published online
by Nature Genetics on April 21, and will appear subsequently in a
print issue of the journal.

Melanoma may appear in places that never see sun, spread to
other parts of the body and become lethal. This type of cancer is not
generally responsive to chemotherapy. According to a report from the
National Cancer Institute, in the United States the incidence rate of
melanoma has more than doubled in the past 20 years.

Chen has been on the track of this gene since her 1995 arrival
at Rutgers, The State University of New Jersey. Her research was
conducted in the Susan Lehman Cullman Laboratory for Cancer Research
at Rutgers' Ernest Mario School of Pharmacy.

"I did not set out to do a melanoma study," said Chen. "All my
life I have been interested in cell transformation and
differentiation. In this case, I was investigating how a fat cell
becomes a fat cell when I observed that one of the mice in my
experiment developed pigmented tumors. Upon further characterization,
these tumors were confirmed to be melanoma."

"After many years of work, we identified a gene that was
involved in these skin abnormalities and went on to prove that it
indeed causes melanoma in the mouse system," said Chen. Surprisingly,
the gene is not a known oncogene - one known to cause cancer - but
one whose normal functions are in the brain.

Chen explained that the expression of a given gene, whether it
is turned on or off, or when, is tightly regulated by many factors.
"It is only in a melanocyte skin cell when the expression of this
particular gene is turned on that it leads to the development of
melanoma," said Chen. "While in the brain, where it is expressed
normally, its functions are associated with learning and memory."

Chen and her collaborators took the next step in this
scientific investigation using human biopsy tissues with various
stages of melanoma. In more than one third of these human samples,
they detected signs of the same aberrant gene expression seen in the
laboratory animals that had melanoma. This confirmed that the gene
involved in melanoma development in the mice is also implicated in
some human melanomas. While there are typically many paths leading to
cancer development, this is a breakthrough in pinpointing one of them
that occurs in both animals and humans.

"We hope to use this knowledge we've gained to investigate
better ways of treating the disease. Early detection is key in
treating melanoma, but malignant melanoma does not normally respond
well to conventional chemotherapy," said Chen. "We need to find more
effective ways to treat the disease. The biggest problem we have is
our inability to target the tumor cells. Most of the treatments
available today affect normal cells, as well. With our understanding
of at least one genetic factor in melanoma, we may now have the
ability to design a new, more specific drug to target that gene or
the protein it expresses," she concluded. Comments (0)

UI study suggests modified tetracycline may help prevent cancer recurrence Posted Sunday, January 26, 2003 by ctustis
Building on previous research, University of Iowa scientists have discovered that a drug already being tested as an anti-cancer agent could potentially be used in conjunction with other cancer therapies to reduce the likelihood of cancer recurrence by targeting the tumor microenvironment.

UI scientists in the laboratory of Mary Hendrix, Ph.D., the Kate Daum Research Professor and head of anatomy and cell biology, previously discovered that aggressive tumor cells can modify their local environment and can induce less aggressive tumor cells encountering this modified environment to become more aggressive. This suggested that in addition to treating tumor cells, changes to the surrounding tissue caused by an aggressive tumor should also be treated to reduce the likelihood of recurrence.

In a study, which appears in the November issue of the Journal Molecular Cancer Therapeutics, the UI researchers demonstrate that a chemically modified tetracycline called COL-3 is able to prevent the altered cellular environment from inducing less aggressive cancer cells to behave more aggressively.

In their earlier studies, the UI team discovered that aggressive melanoma cells produce a molecule called laminin 5 gamma 2 chain and deposit it into their local environment. Enzymes known as matrix metalloproteinases (MMPs) breakdown the laminin molecules and the resulting fragments act as signaling molecules. Less aggressive melanoma cells respond to these signaling fragments and become more aggressive. The fragments of laminin laid down in the environment by the aggressive tumor cells persist in the environment long after the aggressive cells have gone and affect the less aggressive tumor cells that move into the altered environment.

"Standard cancer treatments aim to remove or destroy aggressive cancer cells," said Richard Seftor, Ph.D., lead author of the study and a UI research scientist in Hendrix's lab. "However, we also need to be concerned by the environment left behind by the aggressive cells. We may also need to block these environmental cues."

Chemically modified tetracyclines such as COL-3, are a group of drugs derived from the antibiotic tetracycline that, due to the chemical modification, no longer act as antibiotics. These drugs are powerful inhibitors of MMP enzymes. The research team found that COL-3, blocks the breakdown of laminin to the signaling fragment. It also prevents less aggressive cells from making the laminin molecule in the first place. Additionally, the drug inhibits a process known as vasculogenic mimicry in aggressive melanoma cells. This process is a hallmark of aggressive cancers.

The study results suggest that COL-3 and other drugs like it could be useful in blocking molecular cues residing in tissue surrounding a tumor, and they could be used in conjunction with therapies aimed at destroying aggressive tumor cells.

The study also found that COL-3 was able to reduce the expression of genes associated with vasculogenic mimicry. These results raise the possibility that this drug may be able to suppress this process in aggressive tumor cells, which might reduce the aggressive nature of certain cancer cells.

"These studies provide clear evidence of a successful strategic approach in modifying the tumor microenvironment that may have profound implications in the long term management of cancer," said Hendrix, who also is deputy director of the Holden Comprehensive Cancer Center at UI.

In addition to Hendrix and Seftor, UI researchers involved in the study included Elisabeth Seftor, senior research specialist, and Dawn Kirschmann, Ph.D., assistant research scientist. The study was funded by grants from the National Cancer Institute.

The Holden Comprehensive Cancer Center is Iowa's only National Cancer Institute-designated comprehensive cancer center. NCI-designated comprehensive cancer centers are recognized as the leaders in developing new approaches to cancer prevention and cancer care, conducting leading edge research and educating the public about cancer. Visit the center online at http://www.uihealthcare.com/depts/cancercenter/.
This article is from
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Closing in on a 'Cure' Posted Saturday, September 21, 2002 by ctustis
Sept. 20 - Andy Kilpatrick, a member of the National Honor Society,
didn't dare think about college six years ago. He was in a fight for his
life against melanoma, a very lethal type of skin cancer.

His parents Mary and Tom remember the horrible moment they got the news,
and Andy's first words: "Am I gonna die?"

Her son's cancer was a cruel irony for Mary Kilpatrick. She is a
radiation therapist for cancer patients and she has seen hundreds who
didn't make it. This time, the patient facing death, was her then
15-year-old son.

"I knew how dangerous this was," she says. "I knew melanoma was a deadly
form of skin cancer. I knew that there were not a lot of good treatments
out there for melanoma," she told ABCNEWS' medical editor Dr. Timothy
Johnson.

But for Andy and others like him, there's a new and very promising
treatment in the fight against cancer. And now, the still highly
experimental technique, which harnesses the body's own immune system, is
being developed by researchers for widespread use.

The Cancer Kept Winning

Andy Kilpatrick's cancer not only threatened his life, but scarred him
emotionally and physically from the moment it was first diagnosed with a
pimple-sized tumor on his knee.

"It's [cancer is] my life. And really anything that I remember as
anything I could call my adult life from maybe 15 on, I've been
experiencing my melanoma and treatments with it," he says.

Between treatments, the family was determined to maintain whatever
teenage innocence for Andy they could. But all the while the cancer kept
winning. He developed huge tumors in his pelvis and on his shoulder. At
one point, Andy's doctors discovered the melanoma had spread to his
brain.

Just before surgery to remove the tumor, he said something to his mother
she has never forgotten. "If he didn't make it through, through the
surgery, that, that would be OK, that he'd had a wonderful childhood,"
recalls Mary.

Andy survived the brain surgery but the melanoma continued to grow in
other parts of his body. By now, his best hope was at the National Cancer
Institute with Dr. Steven Rosenberg.

Teaching the Body to Fight Cancer

After 25 years of research, Rosenberg and colleagues at the Institute in
Bethesda, Md., have finally found a way to harness the power of the
body's immune system to fight off this deadly cancer. And some speculate
this new approach could also treat many other cancer types, and possibly
serious immunological diseases such as AIDS.

"I think it's an extremely important advance, and it has the potential
for changing the way we do a lot of cancer therapy," Dr. Alan Rabson,
deputy director of the National Cancer Institute, told Johnson "We're
going to have to see whether it's reproducible in other laboratories, but
I think at this point it looks like it's a major advance."

By using a combination of chemotherapy, hormones, and the patient's own
immune cells, Rosenberg's group successfully shrank Kilpatrick's
malignant tumors, along with the tumors of five others who participated
in the 13 patient trial.

The report "is clearly significant in that it demonstrates a significant
improvement in the response rate for patients with melanoma," concurs Dr.
Lee Riley, Chief of Surgical Oncology at St Luke's Hospital in Bethlehem,
Pa. "This is even more impressive considering most of these patients
already failed very aggressive chemotherapy or immunotherapy treatments."

The treatment approach used in the study is part of what scientists call
immunotherapy, which uses drugs, hormones, cells, vaccines, and even gene
therapy in an attempt to coax the body's own immune system into action to
combat disease.

Similar experiments harnessing the body's own immune system have been
tried before but have not come close to this level of success.

Several Treatment Strategies

The new therapy's success lies in the combined use of several treatment
strategies.

"We start by destroying the body's own immune system of the cancer
patient that's not doing the job. We then replace it with the patient's
own cells that we've previously removed and 'educated' outside the body
so that the cells can attack and destroy the cancer," Rosenberg explains.

Specifically, tumors from each patient were removed surgically and the
tissue treated in the lab to separate out the special lymphocytes - white
blood cells - that can recognize and destroy the tumor.

While these fighter cells are being grown up in the lab, patients are
treated with two chemotherapy drugs that wipe out the immune system and
prepare the body to accept the new and improved lymphocytes.

When the cells are ready, they are transferred back into the blood of the
patient by transfusion, and interleukin hormones are given to help keep
the cells active and fighting.

Experts also point out that the treatment's success is even more
impressive since all of the patients in the study had been through every
other type of available cancer treatment - chemotherapy, surgery,
radiation - to no avail.

A Life Restored

This new technique came just in time for Andy Kilpatrick who had
plummeted to the threshold of death in the fall of 2000.

"And at that point he was in desperate condition, on narcotics to control
pain, bedridden, swollen extremities, volleyball-size tumor in his
pelvis, jutting out of his shirt," remembers Rosenberg.

The research team decided to try the latest version of their new therapy,
and almost two years later, Kilpatrick is a sophomore at Colgate
University, clear of cancer.

"Seeing Andy just enjoy himself is, is absolutely great. It's the way it
should be," says his father.

Andy agrees. "It's just really great to be able to make long-term plans
once again. Because I couldn't for a really long time."

Treating Skin Cancer and Beyond

Because the therapy is still at the beginning stages of development,
Rosenberg is conservatively wary of raising unrealistic expectations.

"It's certainly the best that we've done, but there are still patients
that don't respond, and some of the patients that do respond, don't
respond completely, and so we certainly have a ways to go, but I think we
have broken through a barrier that we've tried to confront for many
years."

And while all of the responding patients in the study still had
significantly reduced tumors at their last check-ups, the researcher's
don't know how long this regression will last. Ideally, the patient's new
tumor-fighting immune system will hunt out and destroy all the cancerous
tumor cells throughout the entire body, leaving the patient cancer-free.

Rosenberg's team is laboring furiously over new ways to improve the
therapy, which they will test in larger numbers of patients. They also
hope to expand the treatment for people with more common cancers as well,
though the group and other experts acknowledge that this may be a long
and hard road.

"Melanoma may be relatively uniquely responsive to immune approaches
because the body seems to recognize the tumor innately," explains Dr.
Frank Haluska, director of melanoma research at Boston's Massachusetts
General Hospital and the Dana-Farber Harvard Cancer Center in Cambridge,
Mass.

Apparently, not all cancer cells have the specific proteins, called
antigens, that sit on the surface of the cell and act as targets for the
immune system to home in on.

"There's obviously a lot we still don't understand, and we're working
literally around the clock - there's somebody in our lab every minute of
every day working on these problems."

Because of the therapy's difficult, expensive, and highly experimental
nature, it is only available at the National Cancer Institute.

"Every treatment that we give is unique for that individual patient, and
it's quite labor intensive," says Rosenberg.

Despite these limitations, cancer experts remain very enthusiastic about
the future of these findings.

"This is still a very early study with only a limited number of patients,
but if this can be reproduced in other centers, it has the potential to
benefit many patients," says Dr. Jay Brooks, chair of hematology/oncology
at The Ochsner Cancer Institute in Baton Rouge, La.

For more information on cancer and its treatment, call 1-800-4-CANCER, or
click to the NCI's Cancer Information Service"

From ABC News http://abcnews.go.com/sections/living/2020/immuno_cancer_patient_2020_020920.html Comments (0)

New Approach to Replacing Immune Cells Shrinks Tumors in Patients with Posted Thursday, September 19, 2002 by ctustis
A new approach to cancer treatment that replaces a patient's immune
system with cancer-fighting cells can lead to tumor shrinkage,
researchers report today in the journal Science*. The study demonstrates
that immune cells, activated in the laboratory against patients' tumors
and then administered to those patients, can attack cancer cells in the
body. The experimental technique, known as adoptive transfer, has shown
promising results in patients with metastatic melanoma who have not
responded to standard treatment. With further research, scientists hope
this approach may have applications to many cancer types, as well as
infectious diseases such as AIDS.

In the study, 13 patients with metastatic melanoma (a deadly form of skin
cancer) who had not responded to standard treatments were treated with
immune cells produced in the laboratory specifically to destroy their
tumors. The treatment resulted in at least 50 percent tumor shrinkage in
six of the patients, with no growth or appearance of new tumors. Four
additional patients had some cancer growths disappear.

Researchers have tried previously to treat cancer with immune cells but
the cells did not survive well in the body. "In the past, only a fraction
of a percent of the cells we injected were able to survive, and they
would persist for only a few days," said Steven A. Rosenberg, M.D.,
Ph.D., of the National Cancer Institute, the lead researcher on the
study.

Improvements in the way immune cells are generated in the laboratory and
the way patients' bodies are prepared to receive them, however, have led
to dramatically different results. "We have been able to generate a very
large number of immune cells that appear in the blood and constitute a
majority of the immune system of the patient. These persist for over four
months and are able to attack the tumor," Rosenberg said.

The adoptive transfer technique fights cancer with T cells, immune cells
that recognize and kill foreign cells that have invaded the body.
Researchers used a small fragment of each patient's melanoma tumor to
grow T cells in the laboratory, using T cells originally taken from the
patients. Exposure to the tumor activated the immune cells so that they
would recognize and attack cells from each specific cancer.

Once the T cells had multiplied to a sufficient number to be used for
treatment, they were administered to patients. Patients were also given a
high dose of a protein called interleukin-2 (IL-2), which stimulates
continued T cell growth in the body. Prior to the immunotherapy,
chemotherapy had been used to deplete patients' own immune cells, which
had proven ineffective at fighting the cancer. Diminishing the old cells
provided an opportunity for the new T cells to repopulate patients'
immune systems.

Analysis of blood and tumor samples from many of the patients who
responded favorably to the treatment revealed that the administered
immune cells were thriving, multiplying rapidly, and attacking tumor
tissue. T cells activated against melanoma became the major component in
patients' immune systems. They persisted for several months and were able
to destroy metastases throughout the body.

Over time, patients' old immune systems recovered, restoring their
ability to fight infections. Researchers report that among the patients
in the study, only occasional opportunistic infections developed during
treatment.

Other side effects were mild autoimmune disorders. T cells act by
recognizing a protein fragment called an antigen on the outside of the
tumor cells. Antigens found on tumor cells may also be found on certain
normal cells in the body, making them vulnerable to attack. Autoimmune
effects among the patients in the study were mild and easily controlled.

Although the treatment is highly experimental, researchers are optimistic
that it may, in the future, extend beyond the treatment of patients with
melanoma. It should be possible, they say, to raise immune cells that
will recognize and attack many tumor types.

Similarly, the same technique could potentially be used to treat some
infectious diseases, such as AIDS.

* Dudley ME, et al. Cancer regression and autoimmunity following clonal
repopulation with anti-tumor lymphocytes and non-myeloablative
conditioning. Published online on Science Express,
http://www.sciencemag.org/sciencexpress/recent.shtml, Sept. 19,2002.
Source: http://newscenter.cancer.gov/pressreleases/melanomavaccine.html Comments (0)

Immune System Could Be Rendered Irreversibly Powerless.American Chemical Society News Release Posted Tuesday, July 23, 2002 by ctustis
ORLANDO, FL -- Natural killer cells are like the Marines of our immune
system; they have the capability to defend us against a lot of different
threats. But researchers have uncovered a potential counter-threat to
this front-line protection. Our body‚s natural killer cells could be
rendered irreversibly powerless to guard against invading tumors and
viral onslaughts after only a brief exposure to a compound found in some
agricultural pesticides and fungicides.
The findings were presented at the 223rd national meeting of the American
Chemical Society (ACS), the world‚s largest scientific society.

Triphenyltin (TPT) is a compound used in fungicides to protect pecan,
potato and sugar beet crops and in pesticides to guard against Colorado
potato beetles. In tests at Tennessee State University in Nashville, TN,
researchers have found an apparent irreversible inhibition of natural
killer cell function after as little as a one-hour exposure to TPT.

The laboratory tests were the first to ever examine TPT specifically in
human natural killer cells, according to chemistry professor Margaret
Whalen, Ph.D., who oversaw the work. Most other studies involved animal
cell lines, she said during a telephone interview. It‚s also the first
time the irreversible effect has been shown, she added.

The findings were presented by one of the contributing researchers,
Sharnise Wilson, a chemistry major and one of Whalen‚s undergraduate
students.

"The results indicate that brief exposures to TPT can cause persistent
suppression of human immune system function," Whalen emphasized.

Although Whalen thinks that most of the TPT levels that agricultural
workers are exposed to in the field are probably below what her group
tested in the lab, "It‚s hard to know what real-life levels for
phenyltins are," she noted.

In the near future, Whalen, in collaboration with Bommanna Loganathan,
Ph.D., of Murray State University in Kentucky, hopes to test blood
samples of agricultural workers who have been exposed to TPT to see
whether significant quantities of the compound can be measured in their
blood.

A type of lymphocyte cell found in the immune system, natural killer
cells aggressively "fight a viral infection or destroy a cancer cell
before other immune system cells recognize that they are there," Whalen
pointed out. "They are quite important." A one-hour exposure to TPT
"causes about a 50 percent to 60 percent loss of the tumor killing
function of the natural killer cell," according to Whalen.

Even after the TPT is removed, the natural killer cells are unable to
regain their strength, as evidenced by tests by Whalen‚s group with human
leukemia cells.

"Despite the fact that the compound is no longer there, they are still
unable to kill the leukemia cell," Whalen said.
Whalen believes the findings "could explain to some extent why compounds
like this seem to increase cancer risks."

The researchers are currently investigating whether interleukin-2 ˜- a
protein produced by other immune system cells ˜- might help reverse the
inhibitory effect of TPT. "It looks like it can to some extent,"
according to Whalen, but she quickly points out that the study is still
ongoing and there is no conclusive data.

The research is primarily funded by the National Institutes of Health‚s
Minority Biomedical Research Support (MBRS) program.

http://allergies.about.com/library/blacs040902.htm Comments (0)

Skin Cancer Breakthrough ReportedStudy Says Gene Defect Causes Most Melanoma Cases Posted Tuesday, June 11, 2002 by ctustis
Skin Cancer Breakthrough Reported
Study Says Gene Defect Causes Most Melanoma Cases

LONDON (June 10) - Scientists have determined that a spontaneous change in a certain gene is involved in 70 percent of cases of melanoma, the deadliest form of skin cancer, which kills nearly 40,000 people a year worldwide.

Experts say the finding might lead to more effective drugs for melanoma, which accounts for just 11 percent of skin cancer, but is hard to treat once it has spread and accounts for almost all deaths from skin cancer.

Dr. Paul Meltzer, a senior cancer genetics investigator at the U.S. National Human Genome Research Institute called the finding the biggest breakthrough in melanoma research for many years.

The discovery, published Sunday in the online version of the journal Nature, is the first fruit of the Cancer Genome Project, a spin-off of the international Human Genome Project being run by researchers at the Wellcome Trust Sanger Institute in Cambridge, England.

Cancer is the disease that lends itself best to an analysis of the human genome because all cancers are a disease of DNA, said Mike Stratton, head of the Cancer Genome Project, which aims to identify which of the 30,000 human genes are involved in cancer and how.

Genes are made up of a DNA code, represented by a sequence of letters. A mutation occurs when the order of the letters changes.

Mutations can be acquired in two ways: either when DNA is damaged by such toxins as radiation, chemicals or viruses, or when mistakes are made before cell division.

Each cell in the body contains a copy of the genome, and duplicates it before it divides into two. The copy isn't always perfect.

Most of the mutations are harmless. However, sometimes a mutation will occur in a particular cell in a key gene and the result will be that the gene will be either switched on or switched off.

That cell will then start to behave abnormally. It will divide when it should stop dividing. It will move out of its usual position in a tissue and may even float off into the bloodstream and deposit in another organ.

That is how cancer evolves. Experts estimate it takes about 25 years from the first gene mutation for a tumor to appear in an adult.

``With the human DNA sequence now available to us, we have started the lengthy and daunting task of trawling through the vast tracts of genome, gene by gene, to see if we can find the abnormal genes that drive cells to behave as cancers,'' said Dr. Andy Futreal, a leader of the Cancer Genome Project.

Meltzer, who was not involved with the research, said the melanoma finding raises great hopes that the ambitious Cancer Genome Project will pan out.

The scientists start by looking at the genes in 48 tumor samples comprising six common cancers. They take each one of the 30,000 genes of the human genome in each sample and look for abnormalities.

After that, they look at the suspect genes in a further 1,000 samples of cancerous tissue, derived from nearly every type of human cancer, to see how important a role the gene mutation plays.

The first abnormality they have found is in the gene called B-RAF, which is one of a chain of genes that must all be switched to the ``on'' position for a cell to grow and divide.

Normally, it switches on and off, but the scientists found that the mutation makes the gene stay switched on all the time and ignore prompts to turn itself off. The cells with the mutation keep multiplying unchecked, leading to cancer.

The researchers found that the code letters in the B-RAF gene were shuffled in 70 percent of melanoma cases, making it the most frequently messed up gene in melanoma.

The scientists also found that about 10 percent of colon cancers had mutations in the B-RAF gene and less frequently in a variety of other cancer types.

Stratton said that because the B-RAF mutation was found in 70 percent of melanoma cases and because the fault in the gene is so specific, it is a promising target for a new melanoma drug, which would be designed to switch off the gene only in cells with a mutated version.

``We're very excited, but we have to temper that with a certain amount of caution. Cancers are devious beasts, they are unpredictable beasts. They don't always respond in the way we would like them to,'' Stratton said. ``We should be optimistic but we should recognize that the path will take several years.''
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Approach promising for melanoma Posted Tuesday, April 16, 2002 by ctustis
Genetic technique may work for other
cancers as well By Ed Susman SPECIAL TO MSNBC

SAN FRANCISCO, April 4 — For years scientists have been trying to use a
biotechnological approach known as “antisense” to treat human cancers.
Now researchers here at a meeting of the American Association for Cancer
Research say they have been able to produce a complete response — total
disappearance of the tumor — in advanced melanoma, a difficult to treat,
fatal disease.
THE SYNTHETIC “antisense” molecule incorporates itself into a gene
responsible for key functions of the cancer cell, essentially disabling
it and preventing it from operating properly. “To our knowledge, this is
the first demonstration of clinical response using an antisense-based
therapy for solid tumors,” said Dr. Burkhard Jansen, an associate
professor of clinical pharmacology at the University of Vienna. Although
the first tests of the therapy were designed simply to establish the best
dose and establish safety, Jansen said one 90-year-old woman who was
given the antisense compound — dubbed G3139 — has been free of disease
for more than two months. In two other patients, tumors shrunk by more
than half, and in another three, tumors visibly decreased.

The average survival for the 14 patients in the study — all of whom had
exhausted standard chemotherapy efforts to control the disease — is nine
months, said Jansen. Typically, the advanced patients would be expected
to die in less than six months, he said. “This is a very exciting
development,” said Dr. Peter Jones, director of the University of
Southern California Norris Comprehensive Cancer Center in Los Angeles.
“We have all been waiting for this type of use of antisense. The study is
very encouraging.”

In the experimental therapy, researchers targeted the bcl-2 gene. In
patients with certain cancers, including melanoma, the gene produces a
chemical shield that protects tumors from chemotherapy. By not allowing
the gene to function properly, anticancer drugs were able to attack the
tumor. At a news briefing, Jansen explained that in the treatment
regimen, patients are given G3139 intravenously for five days, after
which they are administered dacarbazine (DTIC), a standard chemotherapy
agent. In advanced melanoma, DTIC is usually no longer effective against
the disease. The procedure is repeated each time DTIC is given, with some
patients receiving 10 cycles of the drug, he said. Jansen said G3139 was
well-tolerated, even by the 90-year-old. And researchers still have not
reached a maximum dose at which toxicity is great enough to halt
treatment.

Melanoma is a deadly form of skin cancer that strikes 25,800 people in
the United States a year; it is responsible for 24,000 deaths a year. The
manufacturer of G3139, Genta Inc., of Lexington, Mass., is planning to
begin a larger study of the drug with about 270 patients to be recruited
in the United States, Canada and Europe. “What is exciting about this
concept is that bcl-2 is overexpressed in a number of cancers,” Jansen
said. “Lymphoma, colon cancer, lung cancer and breast cancer could be
potential targets for this strategy.”

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Drug shows early promise against melanoma Posted Monday, April 8, 2002 by ctustis

By Jacqueline Stenson

NEW YORK, Apr 08 (Reuters Health) - Preliminary research suggests an
experimental drug may help treat and possibly even stave off the
deadliest form of skin cancer.

"We've made observations with Apomine that are very encouraging for
the prevention and treatment of melanoma," said Dr. Marianne B.
Powell, a researcher at Stanford University School of
Medicine in California. "Alone, it will probably not be the optimal
treatment, but in combination with other drugs it may have some
potential."

If the research pans out, the drug also might one day be included in
sunscreen to help prevent the development of skin cancer, Powell told
Reuters Health.

In a new study of nine patients with advanced melanoma that had
spread despite treatment with surgery and chemotherapy, three
responded to the drug, also known as SR45023A, and their
disease has not worsened. One of these patients has been on the oral
treatment for 3 years so far, according to findings released Monday
at the annual meeting of the American Association for
Cancer Research in San Francisco, California.

However, the disease did worsen in the remaining six patients, Powell
said, so it is unclear just how much of a role the drug actually
played in helping those three patients for whom the disease
did not progress.

"I can't tell you that the drug did it," Powell said.

This preliminary study, conducted at the Arizona Cancer Center, was
designed to test only the safety of the drug. Another study intended
to test effectiveness is currently under way with US
patients and results are due out later this year.

An estimated 53,600 Americans will be diagnosed with melanoma this
year and 7,400 will die from the disease, according to the American
Cancer Society.

Apomine, made by Ilex Oncology, is thought to work against melanoma
by decreasing the activity of Ras, a protein required for the growth
of many melanomas as well as some other cancers.

More specifically, the drug, which was originally developed as a
cholesterol-lowering agent but never came to market for this purpose,
interferes with an enzyme called HMG-CoA reductase
that is important for the production of cholesterol, according to
Powell. It causes cells to make fewer byproducts of cholesterol
synthesis called isoprenoids, which activate the Ras protein. So
with fewer isoprenoids, Ras activity is decreased as is life support
to the tumors, she explained.

It is unclear whether other cholesterol drugs on the market would
have the same effect, though that is a possibility, she said.

Powell said much of the optimism about Apomine comes from laboratory
studies in mice. Her team has found that melanoma tumors shrank when
the drug was applied to the animals' skin.

And in disease-free mice genetically engineered to be susceptible to
melanoma that were exposed to a cancer-causing agent, drug
application reduced the incidence of melanoma by 55%.

Research also has indicated that Apomine helps prevent some of the
DNA damage that results from sun exposure and can lead to melanoma,
Powell said.

Another trial is under way to test the effectiveness of Apomine for
patients with advanced breast cancer.

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Nerves do grow in tumours: study Posted Monday, February 18, 2002 by ctustis
BERLIN, Feb 14 (Reuters Health) - Although doctors have generally thought
that tumors lack nerves, German researchers are building a body of
evidence showing that nerves are in fact present in tumours, which could
lead to a new understanding of cancer.

Dr. Peter Seifert of the University Eye Clinic in Bonn, Germany, first
found nerve fibres in tumours of the eye while using a very high-powered
microscope to examine the tumours.

"People were not looking for nerves in tumours," he said, adding that
most researchers looking at tumors used microscopes that do not show
nerve fibres. "This was the first time nerve fibres were found in
tumours," he said. "But because the eye is such a complicated organ I
decided to look for some kind of proof that the nerve fibres were solely
concerned with the tumour, not the organ."

The proof he needed was eventually found in bladder tumours from five
different patients.

"The tumours there grow into the bladder like a little tree," he said.
"There could be no doubt that the nerve fibres I found there were only
concerned with the tumours."

He has now found more evidence of innervation, in another kind of eye
tumour called choroidal melanoma. This latest research has been accepted
for publication in an American journal for May 2002.

Initial inspection suggested that the nerves in the tumours are involved
in the body's autonomous nervous system--which regulates breathing, heart
rate and many other fundamental systems that are controlled
unconsciously--Seifert said.

"It is possible that this is connected to psychological factors, such as
stress, being influential on tumours," Seifert said. "I personally would
not rule out that this could be the reason. It could also be part of an
explanation of spontaneous healing of tumours, and that some appear and
then go away again."

The next step is to prove that the nerve fibres are carrying messages
from the nervous system, he said.

"It now needs to be researched why the nerve fibres are there--what are
they there to communicate? If you look at a tumour as a system that you
have to fight, you can only do that when you understand it properly,"
Seifert said. "I hope this brings us one small step further in that
direction."

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Tissue Engineering Posted Monday, February 18, 2002 by ctustis
A leading surgeon in the US has told BBC News that he is ready to perform
the world's first transplant of an artificially grown organ.

Dr Anthony Atala, of the Boston Children's Hospital, says he hopes to put
a laboratory-engineered bladder into a patient once he has obtained the
necessary regulatory approval.

He believes permission for the procedure, which has been pioneered in
dogs, will come within the next few months.

Dr Attalla says that if he is successful with the bladder transplant, he
will attempt to repair damaged hearts with new muscle and possibly even
try to grow a kidney.

Polymer ball

"I think over time there will be no limit," Dr Atala said. "I think it is
just a question of figuring out all the different tissue types and cell
types and how they work best, but eventually I think that following the
same strategies just about every organ in the body will be repairable at
the very least."

It was exactly two years ago that a team from the Laboratory for Tissue
Engineering at the Children's Hospital and Harvard Medical School in
Boston announced that it had successfully implanted six beagle dogs with
lab-grown bladders.

Tissue samples were taken from the animals' original bladders and these
were used to cultivate the muscle cells and special bladder skin cells,
called urothelial cells, needed to construct the artificial organs.

The multiplying cells were shaped into beagle bladders by bedding them
down over polymer balls. Transplanted into the dogs, these lab-grown
organs allowed the animals to urinate normally.

Important ally

Dr Atala believes his technique is sufficiently well developed that it
could be used to treat a young child.

A lab-grown bladder could be the answer for a patient whose own organ has
been destroyed by cancer or damaged by an infection or injury.

Dr Atala is seeking approval for human trials from the US Food and Drug
Administration.

Although tissue engineering has huge potential, Dr Atala believes there
will always be a need for donor organs. "I think tissue engineering is
just another solution but it should help reduce the number of patients on
a transplant list."

And, he believes, tissue engineering will prove to be a useful ally to
the emerging field of stem cell medicine, in which "young" cells are
injected into ailing tissue to regenerate it.

"For example, with a patient who has a failing heart, where obviously it
would be very hard to get a biopsy because they would not tolerate the
procedure; then I think stem cells would be the ideal answer."

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Exercise may benefit cancer patients: report Posted Monday, February 18, 2002 by ctustis
NEW YORK, Feb 18 (Reuters Health) - Several studies suggest exercise may
give an immune system boost to cancer survivors, but more research is
needed to see if this translates into a lower risk of cancer recurrence,
according to Canadian researchers.

Of the six studies they reviewed, four showed that patients who followed
a supervised exercise plan during or after cancer treatment had certain
improvements in immune system function.

However, the researchers reported in a recent issue of Cancer, problems
with the studies' designs make it difficult to draw conclusions from the
findings.

"Additional research is needed to determine if physical exercise in
cancer survivors may reduce the risk of cancer recurrence and secondary
malignancies and increase survival times," according to Adrian S. Fairey
and colleagues of the University of Alberta in Edmonton.

But even though the impact of exercise on cancer patients' immune systems
is unclear, there is evidence that supervised activity can lessen some of
the physical, psychological and emotional symptoms related to cancer and
its treatment, Fairey told Reuters Health.

But, the investigator noted, "the majority of physicians are probably
unaware of the benefits of exercise in cancer survivors. This is likely
due to the fact that researchers have only recently begun to examine the
utility of exercise."

The studies Fairey's team looked at were conducted between 1994 and 2000
and followed the effects of several weeks to several months of supervised
exercise--which included activities such as riding a stationary bike,
walking and resistance-training to build muscle strength.

The researchers found that in four studies, exercising patients showed
some improvement in immune system function, including greater activity or
better function in certain important immune cells. In addition, some
exercisers showed better endurance, less decline in physical performance
and greater muscle strength than patients who did not exercise.

Still, the authors pointed out, the problems with these studies, such as
their small size or short duration, limit the weight that can be given to
the results.

But, Fairey said, "there are larger and better-controlled trials of
exercise and immune system function under way."

SOURCE: Cancer 2002;94:539-551.

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Research Finding Could Lead To Vaccines Against A Range Of Cancers Posted Friday, September 14, 2001 by ctustis
Source:University Of California, Berkeley (http://www.berkeley.edu)

Insertion of a single gene into several different tumors enabled mice to
reject them all, leading scientists at UC Berkeley to hope that the gene
might form the basis for a vaccine effective against a range of cancers.

This simple gene therapy also protected the mice against subsequent
injection of tumor cells that had not been altered, meaning their immune
systems remembered the initial challenge - a necessary step for any
vaccine therapy.

"When we introduced the gene into cells that didn't have it and then
injected the tumor cells into mice, they clearly stimulated a variety of
different elements of the immune system, including natural killer cells
and killer T cells," said David H. Raulet, the Choh Hao Li Professor of
Immunology in the College of Letters & Science at UC Berkeley. "The
response in mice was really very dramatic and unexpected - the tumors
were all uniformly rejected."

He is optimistic that the gene - actually two families of similar genes-
will make an effective vaccine therapy, joining the growing arsenal of
cancer immunotherapies in clinical trials today.

Raulet, along with UC Berkeley postdoctoral fellow Andreas Diefenbach,
graduate student Amanda M. Jamieson and postdoctoral fellow Eric R.
Jensen, report the findings in the Sept. 13 issue of Nature. All arepart
of the campus's Health Sciences Initiative.

The findings hark back to a theory popular a generation ago - that the
immune system constantly surveys the body for cancer cells and killsthem
on sight. Only when the growth of cancer cells outstrips the immune
system's ability to eliminate them do tumors form. The idea fell by the
wayside when scientists found that most cancers were no more common in
mice lacking certain components of the immune system than in normalmice.
More recent studies, however, suggest that the mice used in the first
reports were not entirely immunodeficient, and that cancer is indeedmore
common in immunodeficient mice.

One way the immune system could detect tumors is if cells in the process
of converting into cancer cells put up flags, or protein markers, that
alert the immune system and draw its fire. The protein products of the
genes that Raulet and his team have identified could be one of these
common flags.

"The surveillance theory may be on the rebound," Raulet said. "Theimmune
system may be cleaning up many tumors, but we haven't, until now, hadthe
tools to see this."

Raulet and his laboratory colleagues found the proteins while pursuing
their main interest, natural killer cells. These generalized attackcells
of the immune system are among the first and fastest line of defense
against invading tumors and viruses and keep them at bay until the more
specialized T and B cells have had a chance to ramp up production.

While searching for proteins that activate the NKG2D receptor on natural
killer cells, the researchers came across two families of proteins -
called H60 and Rael - that bind the receptor and stimulate naturalkiller
cells to kill as well as secrete gamma-interferon, a cytokine that
activates other cells of the immune system.

Interestingly, the NKG2D receptor is also found on two other immunecells
- macrophages, which engulf and eat invaders, and CD8 "killer" T cells.
Last year, Raulet and his team reported in Nature Immunology that tumor
cells producing the H60 and Rae1 proteins trigger macrophages to switch
to attack mode.

What intrigued Raulet the most, however, was that the proteins werefound
on most cancer cells tested, but not on normal cells. Apparently, the
protein flags are often at such low levels on tumor cells that they fail
to trigger an effective response by natural killer cells or macrophages.
Perhaps, he thought, boosting the amount tumors produce would tip the
scale.

To test this, Diefenbach put the genes for H60 and Rae1-Beta in separate
retroviruses able to shuttle the genes into cells, and used them to
transform three different kinds of tumor cell lines that do not normally
display the
proteins: a melanoma (skin cancer), a T cell lymphoma and a thymoma
(cancer of the thymus). He then injected them into laboratory mice at
levels that would typically kill them.

All mice injected with transformed cells survived, while none of those
injected with untransformed tumor cells survived. They were surprised,
however, to find that the survivor mice developed long-lasting immunity
to the tumor cells. When these mice were injected 8-12 weeks later with
the same tumor cells but lacking H60 and Rae1-Beta, the mice were ableto
successfully fight off the cells. This protective immunity was mediated
by CD8 "killer" T cells.

"We didn't expect protective immunity like this," Diefenbach said. "That
and the immune specificity are hallmarks of a T cell response."

Even more surprising was that the immunity was effective against a
melanoma cell line that is normally unable to induce even a weak immune
response.

Raulet suggests that one reason the immune system is unable to eliminate
some tumors entirely is that it unwittingly selects for cells that
express low levels of the protein marker the immune system homes in on.
That is, tumor cells expressing high levels of the markers are quickly
cleaned out, leaving only cells that slip beneath the radar of natural
killer cells, macrophages and T cells. These cells then grow unchecked.

"A good therapeutic approach could be to engineer the tumor to produce
very high levels of the ligand, to get a strong immune response against
it," Raulet said. "This may combine well with other immunotherapiesbeing
used to get the immune system jazzed up."

He cautioned that clinical trials must determine if the approach will
work in humans.

The team is continuing its studies to see if the technique works as a
cancer therapy. They have achieved encouraging preliminary results by
injecting both transformed and untransformed tumor cells at the same
time, and eventually will test the effect of injecting the transformed
cells into mice that already have established tumors.

The research was supported by the National Institutes of Health.

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Study Shows Antioxidants Play Vital Role In Protecting Skin Posted Tuesday, September 4, 2001 by ctustis
CHAMPAIGN, Ill. - Sun-worshippers beware: Most sunscreen products offer
inadequate protection against the harmful effects of the sun's
ultraviolet radiation.

But there is hope, says a University of Illinois researcher who developed
a technique to peer into the skin and study how it is affected by
ultraviolet radiation. The addition of antioxidants such as vitamins E or
C can help prevent skin cancer and keep skin firm and young looking.
"Ultraviolet radiation is known to cause several forms of skin cancer,
including basal cell carcinoma, squamous cell cancer and deadly
melanoma," said Kerry Hanson, a postdoctoral research scientist in the
UI's Laboratory for Fluorescence Dynamics. "But many important questions
remain, such as in which layers of the skin, and in which parts of skin
cells, the initial damage occurs."

Sunscreens with a sun protection factor of 15 can block up to 94 percent
of the ultraviolet light, Hanson said, but the residual light that does
penetrate the skin can create free radicals - highly reactive molecules
that can weaken or destroy cell membranes. Free radicals can also damage
DNA, create age spots and wrinkles, and depress the immune system,
increasing the risk of skin cancer.

To study the effects of ultraviolet radiation on free radical generation
and the role this plays in skin damage, Hanson employs a two-photon laser
fluorescence-imaging microscope. She images the skin at varying depths
after ultraviolet exposure, looking for fluorescent tags that reveal the
presence of free radicals. She also looks for resulting damage in the
skin cells.

Using the technique, Hanson found that the stratum corneum - the skin's
main protective barrier against environmental assault - generated a
tremendous number of free radicals when exposed to ultraviolet light.
"These free radicals caused considerable damage to both the cytoplasm and
the lipid matrix," she said. "The cytoplasm of the lower epidermis was
also dramatically damaged."

While typical sunscreens offer no protection against free radical damage,
the addition of antioxidants could significantly reduce the generation of
free radicals. In a recent study, Hanson examined the quenching
effectiveness of three antioxidants: vitamin E acetate, vitamin E alcohol
and sodium ascorbyl phosphate (stable vitamin C).

"Vitamin C was by far the best quencher," she said. "There are natural
enzymes in your skin that cleave the phosphate group and form a reservoir
of vitamin C. The best results were achieved after multiple applications
of the antioxidants when a significant amount of vitamin C accumulated
within the skin. Any free radicals that are generated will be quenched by
the vitamin C stored in your skin."

Skin cancer - caused by repeated sunburn - can develop over a lifetime,
Hanson says. "So, the next time you are going out to bake in the sun,
wear plenty of sunscreen. And use one that has an antioxidant."

Hanson will present her findings at the Eighth Biennial Sunscreen
Symposium, to be held Sep. 13-16 in Orlando, Fla.

The Cancer Research Foundation of America and the Skin Cancer Foundation
funded the work.

Note: This story has been adapted from a news release issued by
University Of Illinois At Urbana-Champaign for journalists and other
members of the public. If you wish to quote from any part of this story,
please credit University Of Illinois At Urbana-Champaign as the original
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Aggressive Tumor Cells Leave A Trail In Their Environment That AffectsThe Spread Of Cancer Posted Tuesday, September 4, 2001 by ctustis
IOWA CITY, Iowa - The environment around and between cells is known as
the extracellular matrix and is full of molecules that play important
roles in how tissues look and behave. In a new study, University of Iowa
researchers and their collaborators have shown that highly aggressive
melanoma cells interact with this matrix differently than less aggressive
melanoma cells. These differences may have important implications for the
diagnosis and treatment of melanoma, as well as other types of aggressive
cancers.

The researchers found that aggressive melanoma cells lay down a molecular
track as they interact with their extracellular matrix. These tracks
appear to contain information and cues which, like bread crumbs on a
path, contain information and directions that can be interpreted by less
aggressive tumor cells. These cues may persist in the matrix long after
the aggressive tumor cells have moved on and then cause less aggressive
cells, which move into this area, to become more aggressive.

The UI team, led by Mary J.C. Hendrix, Ph.D., the Kate Daum Research
Professor and head of anatomy and cell biology, and deputy director of
the Holden Comprehensive Cancer Center at the UI, collaborated with
researchers at the Scripps Research Institute in La Jolla, Calif., and
researchers at the National Human Genome Institute and the National
Cancer Institute, both parts of the National Institutes of Health, in
Bethesda, Md.

Their research findings are reported in the Sept. 1 issue of the journal
Cancer Research. Images from the study are featured on the cover of the
journal.

"We wanted to know what these aggressive cancer cells were doing to their
extracellular matrix environment," said Richard E. B. Seftor, Ph.D., a
research scientist in Hendrix's laboratory and lead author of the paper.
"We found that aggressive melanoma cells could alter their environment
and cause other less aggressive melanoma cells to act more aggressively."

Similar to the example of remodeling your house, cells remodel their
extracellular environment by both knocking down and building up the
physical structure they live in. One of the fundamental building blocks
of the extracellular matrix is produced by cells and is a family of
proteins called laminins.

Other proteins produced by cells, called matrix metalloproteinases
(MMPs), act to break down and remodel the extracellular matrix. The
interplay of building up and breaking down the extracellular matrix by
cells plays a major role in how wounds heal, how cancer spreads through
the body (metastasis) and how the body deals with inflammation.

Certain members of the MMP family of proteins contribute to the
aggressiveness of cancer cells. MMPs are important in helping tumor cells
leave a primary tumor and move into and out of the body's blood (and
lymph) vessels. After entering these vessels, tumor cells can travel to
distant parts of the body and begin growing in new tissues.

The ability to spread through the body and invade new tissues are two
features that define a more aggressive and dangerous cancer. Furthermore,
aggressive tumor cells can mimic other cell types, such as the cells that
form vascular networks in the body (a process called vasculogenic
mimicry), while less aggressive tumor cells do not form these networks.

"Our investigation aimed to define the intricate interactions between
certain matrix metalloproteinases produced by the aggressive cancer
cells, and a specific extracellular matrix molecule called laminin 5,
gamma 2 chain," Hendrix said. "We found that this particular laminin is
produced almost exclusively by aggressive, compared to poorly aggressive,
melanoma cells. Furthermore, two specific MMPs (MMP-2 and MMP-14) were
also found to be at higher levels in the aggressive cells."

The study showed that interactions between these two MMPs and this
particular laminin protein, made by the aggressive tumor cells, resulted
in a breakdown of the laminin into fragments that were deposited into
discrete tracks in the extracellular matrix. However, if the MMPs were
prevented from breaking down the laminin protein, then the aggressive
tumor cells could not engage in vasculogenic mimicry.

A key finding was that if the aggressive melanoma cells were grown on the
matrix for only a short period of time and then removed, less aggressive
melanoma cells put onto this matrix were induced to engage in
vasculogenic mimicry. It became apparent that the fragments of the
laminin laid down in the matrix by the aggressive tumor cells were
directing the activity of the less aggressive tumor cells that followed.

"These findings show the importance of specific interactions of
particular molecules in the matrix to support and perpetuate invasion and
migration of tumor cells long after the original aggressive tumor cells
have passed through the matrix," said Hendrix. "The implications of this
study suggest that the matrix of tumors might serve as an excellent
target to inhibit tumor cell signals, which control invasion and
metastasis."

"In addition to finding ways to treat cancer cells themselves, we also
have to be concerned with how aggressive cancer cells alter their
extracellular matrix and the effects this might have on subsequent
populations of less aggressive cells, which come into this environment,"
Seftor added.

In addition to Hendrix and Seftor, the UI researchers on the team
included Elisabeth A. Seftor and Lynn M. G. Gardner. The Scripps Research
Institute researchers included Vito Quaranta, M.D., and his colleagues,
Naohiko Koshikawa, Ph.D. and Martin Bilban, Ph.D. Paul Meltzer, M.D.,
Ph.D., of the National Human Genome Research Institute and William G.
Stetler-Stevenson, M.D., Ph.D., of the National Cancer Institute were
also part of the research team.

The research was funded by grants from the National Cancer Institute.

University of Iowa Health Care describes the partnership between the UI
College of Medicine and the UI Hospitals and Clinics and the patient
care, medical education and research programs and services they provide.
Visit UI Health Care online at http://www.uihealthcare.com

Note: This story has been adapted from a news release issued by
University Of Iowa for journalists and other members of the public. If
you wish to quote from any part of this story, please credit University
Of Iowa as the original source. You may also wish to include the
following link in any citation:
http://www.sciencedaily.com/releases/2001/09/010903091625.htm
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Scientists Find Gene That May Be Key to Onset of Deadly Skin CancerThursday, August 16, 2001 Posted Friday, August 17, 2001 by ctustis
BY TROY GOODMAN THE SALT LAKE TRIBUNE

Scientists analyzing various kinds of moles say they have pinpointed a
key gene heralding the transformation of a blemish from non-threatening
into melanoma, the deadliest type of skin cancer. The research by a Johns
Hopkins University team holds promise in the development of early
diagnostic markers for the rapidly-spreading disease, Utah cancer experts
said. Early treatment of melanoma is crucial for survival since less than
10 percent of people with a developed stage of the disease live beyond
five years. "Telling the difference between precancerous moles and
early-stage melanoma can be very difficult," said Rhoda Alani, an
oncology and genetics professor at Johns Hopkins in Baltimore and author
of the study. "If it's melanoma, you want to catch it very early and
treat it aggressively by removing as much tissue as possible to cure the
disease." Alani, along with a three-person research team, found that
melanomas contain a regulatory gene known as Id1, which acts like a DNA
accelerator to fuel cancer cells into uncontrollable growth. The presence
of Id1 in suspect moles could help doctors spot early melanoma and then
treat it while it's still at a curable stage, Alani said. The research
appears in the latest issue of Cancer Research, a journal of the American
Association for Cancer Research. It was based on 21 samples of skin
lesions, all in varying forms of non-malignancy or malignancy. The
findings caught the interest of Salt Lake City-based Huntsman Cancer
Institute where hundreds of melanoma patients -- all victims of Utah's
sun-drenched high-altitude atmospheric conditions -- are studied every
year for their skin cancer. Sancy Leachman, director of Huntsman's
familial melanomal research clinic, said the latest study holds promise.
The findings build on earlier research conducted at the University of
Utah and Salt Lake City biomed company Myriad Genetics during the early
1990s. Back then, Leachman said, the U. and Myriad were key players in a
skin cancer breakthrough that identified biological changes in another
gene, called p16, that led to melanoma formation. Today, those findings
are part of a widely held belief that "about 40 percent of the familial
melanoma is because of the p16 gene," Leachman said. But familial
melanoma, the results of an inherited predisposition to getting the
disease, isn't the only explanation. Sun overexposure, fair complexions
and occupational exposure (to coal tar, pitch, creosote, radium, for
example) also play a part, she said. This year alone, melanoma will
strike more than half a million Americans and kill some 7,800, according
to the research association. So the Cancer Research study on Id1, a gene
that regulates p16 action, sheds light on the genetic "pathway" cells
cross when they go from normal to cancerous, Leachman said. But knowing
more about that pathway could be less important than further research on
p16's direct role in melanoma formation. "It might be more important to
focus on p16 itself," she said of the Cancer Research findings. Still,
hopes for better genetic tests that could spot early skin cancer growths
were on the minds of the Johns Hopkins researchers when they wrote the
latest study. "Marker studies for Id1 in melanocytic lesions of uncertain
malignant potential may play a critical role . . . and may help determine
the appropriate treatment and prognosis of melanocytic lesions," the
authors wrote.

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Genetic Mutation May Be Key To Onset Of Deadly Skin Cancer Posted Friday, August 17, 2001 by ctustis
A Johns Hopkins scientist and a team of collaborators have discovered how
precancerous moles may progress to melanomas, the most deadly type of
skin cancer. The preliminary report, in the August 15 issue of Cancer
Research, describes a link between two genes that trigger skin cancers
and could serve as early diagnostic markers for the disease. The
researchers say that, in melanomas, a cell growth regulatory gene known
as Id1 deactivates an important tumor suppressor gene (p16/Ink4a),
allowing cancer cells to grow uncontrollably.* High levels of Id1
proteins are found only in the first stages of melanoma, allowing it to
be detected and treated while still in a curable stage. trigger skin
cancers and could serve as early diagnostic markers for the disease.

"Telling the difference between precancerous moles and early-stage
melanoma can be very difficult, and the treatments for these two lesions
differ significantly," explains Rhoda Alani, M.D., assistant professor of
oncology, dermatology, molecular biology and genetics and director of the
study. "If it's melanoma, you want to catch it very early and treat it
aggressively by removing as much tissue as possible to cure the disease."
Since Id1 is expressed in early-stage melanoma, it has the potential to
serve as a definitive diagnostic marker although more studies are needed
to confirm this use.trigger skin cancers and could serve as early
diagnostic markers for the disease.

The scientists studied Id1 protein expression in 21 tissue samples from a
variety of skin cancers, including normal non-cancerous moles (benign
nevus), precancerous moles (dysplastic nevus), early-stage melanoma
(in-situ melanoma), invasive melanoma and metastatic melanoma. "We found
high levels of Id1 activity in the earliest phases of melanoma, when it's
limited to the top layer of the skin (or epidermis). Precancerous moles,
invasive and metastatic melanomas do not express high levels of Id1,"
reports Alani. Larger studies are planned.trigger skin cancers and could
serve as early diagnostic markers for the disease.

The scientists speculate that while the Id1 gene shuts off p16/Ink4a in
early melanomas and lifts the brake on uncontrolled cancer cell growth,
various mutations or other DNA changes must also occur to the p16/Ink4a
gene to damage it beyond repair. So, as the cancer progresses, Id1
becomes less important for shutting off the gene. "This may explain why
we see lower expression of Id1 in more advanced melanomas," says
Alani.trigger skin cancers and could serve as early diagnostic markers
for the disease.

Melanoma can progress very rapidly and spread to other parts of the body.
When treated early, the chance for cure is very high. Only 12 percent of
people with metastatic melanoma survive beyond five years.trigger skin
cancers and could serve as early diagnostic markers for the disease.

Melanoma will strike 51,400 people in the United States this year, and
7,800 will die from the disease.trigger skin cancers and could serve as
early diagnostic markers for the disease.

In addition to Alani, other participants in this research include David
Polsky from NYU Medical Center; Alison Zuyung Young and Klaus J. Busam
from Memorial Sloan-Kettering Cancer Center. This research was funded by
The National Institute of Arthritis, Musculoskeletal and Skin Diseases
(NIAMS).trigger skin cancers and could serve as early diagnostic markers
for the disease.

Note: This story has been adapted from a news release issued by Johns
Hopkins Medical Institutions for journalists and other members of the
public. If you wish to quote from any part of this story, please credit
Johns Hopkins Medical Institutions as the original source. You may also
wish to include the following link in any citation:
http://www.sciencedaily.com/releases/2001/08/010815082241.htm
Source:Johns Hopkins Medical Institutions (http://www.hopkinsmedicine.org/)

Date:Posted 8/16/2001 Comments (0)

NASA looks at ultraviolet radiation Posted Friday, August 17, 2001 by ctustis
August 15, 2001 Posted: 3:38 PM EDT (1938 GMT)

ATLANTA, Georgia (CNN) -- Scientists from NASA's Goddard Space Flight
Center in Greenbelt, Maryland, pieced together a year's worth of images
from the Total Ozone Mapping Spectrometer (TOMS) orbiting aboard the
Earth Probe spacecraft for a moving glimpse at global ultraviolet (UV)
radiation.

The Earth Probe satellite travels on a polar orbit about 740 kilometers
above the surface, crossing the equator every day at noon local time.
Using measurements of ozone, cloud cover and solar radiation escaping
from the top of the atmosphere, TOMS estimates the amount of radiation
reaching the earth.

The animations, released on Goddard's Web site on Wednesday, show
traveling hot spots focused around the middle of the globe, particularly
during the summer months of the Southern Hemisphere (winter in the
Northern Hemisphere), where cloud cover is thin.

"That's because of the ITCZ -- the Intertropical Conversion Zone," says
Jay Herman, a NASA project scientist at Goddard. "It has to do with the
motions of clouds and the peculiarity of the way land mass is
distributed."

"There are more clear-sky days in the Southern Hemisphere than there are
in the Northern Hemisphere," he says. "Australia has one of the lowest
number of cloudy days than any place on earth, except for South Africa."

Thin air a t higher elevations -- like the Himalayas and the Rockies --
also raises the UV levels, but higher latitudes -- closer to the poles --
counteract that effect.

Use protection

But what does all that mean for the typical earthling?

"If you live in the middle latitudes, where most people live, nothing
much," Herman said. "Protect yourself from the sun. But people living at
higher latitudes are at greater risk than they used to be because of the
ozone depletion."

That would include northern Europe, Canada, and the southernmost portions
of South America and Africa.

Two types of UV radiation -- UVA, which is blocked by glass, and UVB,
which is not -- do the most damage. UVB rays are the primary cause of
sunburn and skin cancer, while UVA rays penetrate deeper in the skin's
base layer, attributing to both cancer and sunburns.

Both rays can damage the body's immune system.

The American Academy of Dermatology (AAD) says that half of all new
cancers are skin cancers -- and that melanoma, a particularly virulent
form of skin cancer, kills one person per hour on average. And while it's
certainly not the only cause of skin cancer, exposure to the sun is
perhaps the most important preventable cause, say dermatologists.

The Food and Drug Administration (FDA) and the AAD recognize six skin
categories, ranging from light-pigmented skin that is extremely sensitive
to the sun's effects to darker-pigmented skin that almost never burns.

But dermatologists say everyone should take precautions when dealing with
the sun, including using a sunscreen that protects against both UVA and
UVB rays and staying out of the sun during the hottest part of the day --
generally 10 a.m. to 4 p.m.

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Notre Dame team is working on genetically engineeredsunscreen to prevent skin cancer. Posted Friday, July 20, 2001 by ctustis
By Gina Barton
Indianapolis Star
July 10, 2001

It's widely known that the best way to protect
yourself from skin cancer is sunscreen.

Researchers at the University of Notre Dame hope they
have taken the first step toward helping people who
haven't followed that advice.

Most people who develop skin cancer severely harm
their skin in their teen years or early 20s, yet the
disease doesn't catch up with them until after age 50.
Although the Notre Dame research is still in its early
stages, scientists there hope their work will help
reverse some of the damage in the intervening years,
before the cancer has a chance to develop.

Skin cancer is the most common type of cancer in the
United States, according to the National Cancer
Institute. About 1.4 million people are diagnosed each
year, and 40 to 50 percent of Americans who live to
age 65 will have skin cancer at least once.

"We're looking at prevention," said Olaf Wiest, a
chemist who is heading up the Notre Dame research
project.

The discovery could some day lead to a genetically
engineered sunscreen.

In humans, sunscreen can block the sun's ultraviolet
rays, thus protecting DNA from damage. Some other life
forms, such as yeast, E.coli bacteria and the South
American possum, have natural protection in the form
of a body enzyme. The enzyme prevents them from
getting cancer and from dying due to sun damage.

Here's how it works. Each DNA molecule is made up of
four base proteins: adenine, cytosine, guanine and
thymine. When too much sun exposure occurs, thymine
proteins from different molecules fuse together,
leading to a precancerous condition. The enzyme uses
electron transfer to break them apart again.

"In one billionth of a second, the repair is made. The
electron jumps over and chemically reconfigures the
DNA," Wiest said.

For more than five years, Wiest and his team have used
these naturally occurring enzymes as a model, trying
to create a new enzyme that will do the same thing in
human DNA. They recently made a breakthrough: their
man-made enzyme has repaired human thymine. The next
step is to try it with complete molecules of DNA. If
that works, the number of skin cancer sufferers could
be greatly reduced.

"I think it's a great concept," said Dr. Debra
Jaliman, a clinical instructor at Mount Sinai School
of Medicine in New York City.

The research is particularly promising because the
sun's damaging ultraviolet light is hard to avoid,
even with today's sunscreens, she said.

Wiest said it is too early in the research process to
tell if his new enzyme will be used commercially, or
even with a doctor's prescription. But if all goes
well, the enzyme could be formulated into a sunscreen
lotion or spray. People could apply it, let it make
repairs, and then wash it away.

"It could be a sunscreen for the day after or for
years after," Wiest said.

This article can be found at
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Animal studies indicate new approach for treating end-stage skin and kidney cancers Posted Monday, March 26, 2001 by ctustis
New Orleans, La., March 26, 2001 - Advanced skin and end-stage kidney
cancer patients may have a better chance of survival with drugs developed
from a new synthetic enzyme that significantly improves the effectiveness
of existing interleukin-2 (IL-2) cancer therapy, based on research
presented today at the American Association for Cancer Research 92nd
Annual Meeting.

In animal studies conducted by researchers at the Huntsman Cancer
Institute in Salt Lake City, UT, and MetaPhore Pharmaceuticals in St.
Louis, MO, the synthetic enzyme M40403 showed an ability to reverse the
extreme blood-pressure drop that is a common side effect of high-dosage
IL-2 cancer therapy. The research also showed that the compound enhances
the anti-cancer properties of IL-2 therapy.

IL-2 immunotherapy, which works by activating natural killer (NK) cells
that have the ability to recognize and destroy many types of tumors, is
an approved treatment for inoperable metastatic melanoma and metastatic
renal cell carcinoma. About 80,000 cases of melanoma and renal cell
carcinoma are diagnosed in the U.S. each year.

IL-2 use is limited, however, by potentially life threatening side
effects, including hypotension, particularly at the high-dosage level
indicated for these end-stage cancers. A majority of patients undergoing
high-dosage IL-2 treatment currently either require intensive care unit
(ICU) intervention and/or are unable to complete the full course of
treatment.

Reseachers administered the synthetic enzyme, which mimics the action of
a natural enzyme, superoxide dismutase (SOD), as a co-therapy with IL-2
in several animal models of advanced cancer. Previous studies have
confirmed that the synthetic enzyme effectively reproduces the
free-radical fighting properties of the natural SOD enzyme, which has
been found to be deficient in cancer states.

When in excess, free radicals - particularly superoxide anions - have
been shown to deactivate a class of molecules, called catecholamines,
which aid the body's natural blood pressure regulatory system. By
reducing superoxide, the synthetic SOD enzyme restores the levels of
catecholamines necessary to constrict blood vessels and reverse
hypotension.

Moreover, superoxide also inhibits the activity of NK cells, hampering
the anti-tumor effect of IL-2.

"By restoring the body's natural vascular regulatory system, the
synthetic SOD enzyme addresses a major limiting side effect of current
IL-2 therapies. It also appears to work synergistically with IL-2's
anti-cancer properties," said Dr. Wolfram Samlowski of the Huntsman
Cancer Institute at the University of Utah.

In two separate animal models, as a co-therapy with IL-2, the synthetic
SOD enzyme prevented the onset of IL-2 induced hypotension and enhanced
IL-2's ability to kill malignant cells. In an animal model of pulmonary
metastasis, both the synthetic SOD enzyme and IL-2 appeared to have
significant anti-tumor action, in combination and individually. In the
aggressive Meth A fibrosarcoma tumor model, co-therapy with IL-2 and the
synthetic SOD enzyme resulted in a 50 percent complete remission rate,
which lasted more than 90 days following tumor implantation, while mice
treated with IL-2 therapy alone lived an average of 21 days following
implantation with no remissions.

"These studies demonstrate that the synthetic SOD enzyme may have
tremendous potential as a co-therapy with IL-2 and related cytokine
cancer therapies," added Daniela Salvemini, MetaPhore's Vice President
and Director of Pharmacology and co-investigator in the study.

Other members of the research team include Ryan Petersen and John Robert
McGregor of the Huntsman Cancer Institute.

Background

Production of superoxide, a free radical, results from cellular oxidative
metabolism. However, when too much superoxide is produced in the body,
various biomolecules, cell structures and even genes are damaged.
Free-radical damage has been linked with a wide range of diseases and
conditions, including autoimmune and neurodegenerative disorders,
multiple types of cancer, complications of diabetes mellitus, strokes,
reperfusion injury, as well as pain and inflammation. One of the body's
primary defense mechanisms against free-radical damage is the superoxide
dismutase (SOD) family of enzymes. These enzymes typically regulate
normal levels of superoxide by converting it into hydrogen peroxide and
oxygen, also reducing production of related damaging free radicals, such
as peroxynitrite.

MetaPhore is developing a proprietary family of drugs that mimic the
catalytic activity of SOD to address the diseases and conditions
resulting from excessive superoxide production. In pre-clinical models,
the lead candidate from this family has suggested the potential to combat
such diseases and conditions more effectively and with fewer side effects
than existing treatments.

"Synthetic SOD enzymes have major medical potential, based on the growing
body of anti-oxidant and disease research. For more than twenty years, we
have understood the free-radical fighting power of the body's natural SOD
enzymes, but until recently, we have been unable to reproduce that
beneficial effect in a stable and selective drug form," said Dennis
Riley, MetaPhore's Senior Vice President of Research & Development.

MetaPhore's synthetic SOD enzyme is well suited for use as a drug because
it has a low molecular weight, is highly stable and does not appear to
elicit an immune response in the body.

Animal studies published in journals such as Science and the Proceedings
of the National Academy of Sciences during the past few years have
confirmed the disease fighting potential of MetaPhore's synthetic SOD
enzymes. These studies have also demonstrated that MetaPhore's synthetic
SOD enzyme substantially reduces tissue damage due to inflammation and
reperfusion injury - the latter involving the return of blood flow
following removal of blockade, such as after an ischemic heart attack or
stroke.

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Cancer Discovery May Speed Treatment Posted Monday, March 26, 2001 by ctustis
Updated 3:27 PM ET March 26, 2001

By DANIEL Q. HANEY, AP Medical Editor

NEW ORLEANS (AP) - Scientists have figured out the precise
three-dimensional structure of a spot where cancer cells receive growth
instructions, a discovery that may speed the development of exquisitely
precise new treatments.

One of the forces that makes cancer grow rampantly is a substance called
insulin-like growth factor, or IGF. Without this hormone, many cancers
will shut down and die.

Researchers have long understood the importance of IGF but so far have
been unable to exploit this knowledge to make new cancer drugs.

The obvious strategy is to block the spot that lets IGF get into cells.
However, this structure, called a receptor, is extremely similar to
another one that serves as the entry point for insulin.

Although normal cells can survive without IGF, they still need insulin.
The difficulty is making a drug that gums up the IGF receptor but not the
lookalike insulin receptor.

On Monday, researchers from Amgen Inc. announced they have deciphered the
3-D crystal structure of the IGF receptor. This means they know exactly
what it looks like down to the last atom.

Scientists already know the structure of the insulin receptor. So now
they can compare the two and look for parts that are unique to the IGF
receptor.

Dr. Xiaotian Zhu described the discovery at a meeting in New Orleans of
the American Association for Cancer Research.

The goal is to craft molecules that will cover up part of this receptor,
destroying its ability to take in chemical signals, without also
disabling the insulin receptor.

"We found quite a few structures that are unique to IGF," Zhu said. "This
could not have been predicted otherwise. We think this will greatly
accelerate the drug discovery process."

Dr. Edward Sausville of the National Cancer Institute noted that many
types of cancer, especially prostate tumors, are fueled by IGF. Blocking
it might be combined with standard chemotherapy as a cancer treatment.
The approach might also be used on patients with precancerous prostate
abnormalities to keep them from turning into cancer.

Development is still early, however, and it is unclear whether IGF
blockers being developed by Amgen will actually work this way.

Sausville said the goal of this and other research is to develop drugs
that are "precisely designed to address abnormalities present in each
individual's tumor."

Such drugs might work with far fewer side effects than standard
chemotherapy, which broadly attacks all rapidly growing cells in the
body.

Zhu said blocking IGF should be safe, since people who have naturally
occurring IGF deficiencies are unusually small but otherwise healthy.

One thing that makes cancer different from normal tissue is that it
refuses to die. Experiments suggest that cancer cells need IGF to escape
the usual limits on the number of times a cell can divide. When IGF is
shut off, cancer cells often simply stop growing and expire.

Among other reports at the meeting Monday:

-Dr. Robert Kreitman of the cancer institute combined an antibody with a
poison made by pseudomonas bacteria. The treatment zeros in on cancerous
blood cells that have unusually large numbers of a protein called CD22 on
their surface. The treatment is showing promise in otherwise untreatable
cases of hairy cell leukemia and chronic lymphocytic leukemia.

-Dr. Brian Ross of the University of Michigan said a scan called
diffusion-weighed magnetic resonance imaging may be able to tell within a
few days whether chemotherapy is working against tumors. The scan reveals
whether water in the tumors is moving more freely, as happens when cells
die. Testing is under way on 12 patients.

-Dr. Sergio Huerta of the UCLA Center for Human Nutrition found
preliminary evidence that a synthetic form of vitamin D might protect
against colon cancer. Ordinary vitamin D produces dangerously high
calcium levels if taken in large quantities. In mice, at least, the
synthetic vitamin reduced the risk of colon cancer with only a modest
calcium rise.

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New Clue To Diagnosis And Treatment Of Malignant Melanoma Posted Monday, January 15, 2001 by ctustis
Cold Spring Harbor, NY -- Malignant melanoma is an aggressive, deadly
cancer that does not respond to conventional chemotherapy. Other
aggressive, chemoresistant cancers - and approximately half of all
cancers - are characterized by mutations in the p53 tumor suppressor
gene. Malignant melanomas, however, do not typically display mutations in
the p53 gene.

To explore alternative explanations for the origins and properties of
malignant melanoma, and to identify potential targets and strategies for
therapy, Scott Lowe and his colleagues at Cold Spring Harbor Laboratory
have examined the status of other genes known to function downstream of
p53 in a pathway leading to "apoptosis" or "programmed cell death." When
intact, this pathway rids the body of abnormal, pre-cancerous cells by
triggering a cellular self-destruct mechanism. When this pathway is
disrupted (by the loss of p53 function, for example), pre-cancerous cells
survive and proliferate resulting in cancer (see figure).

In a study to be published tomorrow in Nature, Lowe and his colleagues
report that malignant melanomas often lose a key trigger of programmed
cell death - a protein called Apaf-1 (apoptosis activation factor-1). The
researchers also discovered that the loss of Apaf-1 in melanoma cells is
associated with resistance to the chemotherapy drug adriamycin. Most
significantly, the study shows that restoring Apaf-1 in melanoma cells
rescues the ability of these tumor cells to kill themselves in response
to adriamycin.

"The loss of Apaf-1 in malignant melanoma is a prime explanation for both
the extreme chemoresistance and the apparent lack of p53 defects in such
cancers," says Lowe.

The study is significant because it demonstrates that accurate diagnosis
and treatment of malignant melanoma, and perhaps other cancers, should
include an assessment of the status of Apaf-1.

Maria Soengas of Cold Spring Harbor Laboratory was the principal author
of the study. The principal collaborators in the study were William L.
Gerald and Carlos Cordon-Cardo of Memorial Sloan-Kettering Cancer Center.

An intriguing aspect of the study relates to the mechanisms that cause
the loss of Apaf-1 in melanomas. The researchers were not surprised to
find that one of the two copies of the Apaf-1 gene was deleted in many of
the melanomas they examined (a well-known phenomenon called "loss of
heterozygosity"). However, the other Apaf-1 gene copy in these cells was
present and apparently normal in terms of its DNA sequence.
Interestingly, Lowe and his colleagues found that complete loss of Apaf-1
was due to "transcriptional silencing" of the remaining, normal copy of
the Apaf-1 gene in melanomas. Transcriptional silencing, or the
suppression of gene expression due to higher order chromatin structure,
is emerging as a principle mechanism whereby Apaf-1 and other tumor
suppressor genes can be inactivated, resulting in cancer when other
copies of such genes are lost, mutated, or similarly silenced.

Scott Lowe is a Professor at Cold Spring Harbor Laboratory and Deputy
Director of the Cold Spring Harbor Laboratory Cancer Center. Other
scientists from Memorial Sloan-Kettering Cancer Center (Paolo Capodieci,
David Polsky, Jaume Mora), Johns Hopkins University and Oncology Center
(Manel Esteller, James G. Herman), and Cold Spring Harbor Laboratory
(Ximena Opitz-Araya, W. Richard McCombie, Yuri A. Lazebnik) contributed
to the study.

Note: This story has been adapted from a news release issued by Cold
Spring
Harbor Laboratory for journalists and other members of the public. If you
wish to quote from any part of this story, please credit Cold Spring
Harbor Laboratory as the original source. You may also wish to include
the following link in any citation:

http://www.sciencedaily.com/releases/2001/01/010111075020.htm


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Rebuttal to FDA Panel Action Posted Friday, December 29, 2000 by ctustis
The following comments originate from an investigator for the Maxamine
clinical trials. It is suggested that if you agree with these comments you are free
to use them when contacting your congressional representative.


1. For a drug to be approved it must be EFFECTIVE and SAFE. There are hedges
to this but this is the bottom line. The ODAC (Oncology Drug Advisory
Committee) for some reason was determined to prove that Maxamine was
neither. We believe that the FDA should look more favorably on a drug that
holds out hope for treating one of the most untreatable cancers known to
man. A cancer that is increasing in incidence faster than any other in the
US. Shouldn't the FDA be looking for reasons to approve, rather than
disapprove, such a drug? Haven't they followed this sort of thinking for
drugs for both breast cancer and AIDS?

2. The drug is flat out safe. My patients have tolerated it extremely well.
The major side effects are actually all from the IL-2, which is approved by
the FDA. Others on the list I suspect can corroborate this point of view.
However, the FDA, to really perform due diligence should seek out physicians
who have treated patients (there were none on ODAC) and patients who have
received Maxamine.

3. The FDA should talk to physicians who have actually treated melanoma
patients. None of the ODAC members seemed to have a good idea of how rapidly
melanoma can progress. One member, from Michigan, stated that he couldn't
believe that so many melanoma patients could deteriorate and die within
twelve weeks when they looked so well on study entry. The FDA needs to hear
how melanoma strikes our loved ones, from those of us who have seen it all
too close at hand.

4. The FDA needs to stop playing statistical games with the data. The drug
works. The survival time of patients treated with Maxamine who had liver
metastases virtually doubled. Unfortunately, it doesn't help everyone, but
neither does interferon, interleukin-2 or DTIC, all of which are approved
for melanoma treatment. The FDA statisticians performed many analyses that
would be argued with endlessly if they had to be published in any medical
journal, or presented at any medical meeting. In other words, they
unilaterally decided what was right, and did not have to answer to anyone
with a real insight into the clinical situation. One of the articles they
based their decisions (about prognostic factors) on was published in 1983!
Seventeen years is an eternity in melanoma care. Yet that same author
published an article in 2000 that said something very different (Balch), and
they ignored its findings.

5. Finally, the FDA complained that there was only a single study that
suggested that Maxamine works. How many comparative studies showed that IL2
worked? Answer:NONE. How many comparative studies showed that
interferon-alfa worked? Answer: when approved, ONLY ONE, and the efficacy
was not consistent between groups. Yet, the FDA approved it for all groups,
and without doing the subset balancing analyses that they played around with
for Maxamine. Further, the FDA approved interferon with a very slim
statistical margin that barely met the required "confidence interval".

As melanoma patients, the physicians who care for them, and their anxious
family members, we want the FDA to do the right thing. We want them to
approve the ONLY drug that has EVER shown ANY survival benefit in any
subgroup of Stage IV melanoma patients; a drug that is safe to administer; a
drug that preserves quality of life while offering hope for the future. Comments (307)

FDA Advisers Reject Histamine Dihydrochloride for Advanced Melanoma Posted Friday, December 29, 2000 by ctustis
BETHESDA, MD (Reuters Health) Dec 13 - Food and Drug Administration (FDA)
advisers on Wednesday unanimously voted against approval of Maxim
Pharmaceutical's Maxamine (histamine dihydrochloride) when given in
conjunction with interleukin-2 for metastatic melanoma.

The Oncologic Drugs Advisory Committee said that due to faulty study
design, the company had not proven that the combination of drugs improved
survival over IL-2 alone. The FDA usually follows its advisory panels'
advice.

According to Maxim, the histamine seems to boost the body's
responsiveness to IL-2, and it has fewer side effects than high doses of
IL-2 alone. Panelists questioned whether the company had adequately
proved how the drug worked, and they were also concerned about patient
deaths in Maxim's pivotal study.

The FDA generally requires two randomized controlled trials for approval,
but will accept one if the data are strong enough. Maxim was asked to
submit two studies and was advised to randomize patients according to
prognostic factors, but the company elected a different path. At the
committee meeting Maxim submitted data from one pivotal phase III study
and presented interim results from an ongoing trial.

In the phase III trial, 153 patients with advanced metastatic melanoma
got IL-2 alone and 152 received the combination. Patients with liver
metastases were not randomized separately, despite the FDA's suggestion
to do so. Kurt Gehlsen, Maxim senior vice president, said he regrets that
decision. As the study progressed, it appeared that patients whose
disease had spread to their liver fared better than those with metastases
at other sites.

There was no statistically significant difference in survival between the
IL-2 arm and the group getting IL-2 plus histamine. But in the 55
patients with liver metastases, median survival was much greater: 283
days for IL-2 plus Maxamine versus 154 days for the IL-2 monotherapy
group, according to the company.

Committee members were encouraged by the difference. "I hope that the
results are true and that a second trial can be done so we can find out
if it is true," said panelist Richard Simon of the National Cancer
Institute. But, he added, given the study design, "I certainly don't find
this even approaches convincing evidence of effectiveness."

Panelists were also concerned about patient deaths. Thirty-three patients
— half on Maxamine — died within 30 days of receiving a drug. Without a
non-IL-2 arm, it could not be determined whether the deaths were due to a
drug or the underlying disease, said FDA reviewer Judy Chiao.

Maxim said that most adverse events were expected and very mild. Patients
experienced flushing, hypotension, tachycardia, headache, and dizziness,
but these symptoms dissipated within a half hour to an hour of the
injections, said the company. Grade 3 and 4 cardiovascular events were
negligible, about 1%. Comments (1)

Interferon Alfa 2b extends overall survival and relapse-free survival inpatients with high-risk melanoma, reports University of Pittsburgh-ledU.S. I Posted Monday, October 16, 2000 by ctustis
Contact: Lauren Ward

wardle@msx.upmc.edu 412-624-2607 University of Pittsburgh Medical Center



PITTSBURGH, Oct. 16 - Interferon alfa 2b (INTRON® A) unequivocally
improves overall and relapse-free survival in adult patients who have
surgically treated melanoma considered at high risk of recurring,
according to results of a definitive study evaluating the use of this
agent and comparing it with one of the best-developed anti-melanoma
vaccines, GMK. Results of this National Cancer Institute-funded study
(E1694), led by John Kirkwood, M.D., at the University of Pittsburgh
Cancer Institute (UPCI), are being presented Oct. 16 at the Presidential
Symposium of the European Society of Medical Oncology in Hamburg,
Germany. *

"This report indisputably proves that high-dose interferon alfa 2b is the
standard adjuvant therapy for high-risk melanoma patients," stated Dr.
Kirkwood, director of the UPCI's Melanoma Center. "It is my hope and
expectation that these results will motivate many more physicians who
treat melanoma to consider aggressive therapy with this regimen, as well
as new clinical trials that build upon this regimen. Doing so could
improve patient outcomes for thousands of individuals," added Dr.
Kirkwood, who also is vice chairman for research at the University of
Pittsburgh's department of medicine.

Study results of E1694 showed that when given at a high dose (20MIU/m2
intravenously and 10MIU/m2 subcutaneously), interferon alfa 2b extends
overall survival in surgically treated patients, as well as relapse-free
survival, or the amount of time free of disease recurrence. Patients who
received the GMK vaccine, by contrast, showed significantly lower overall
survival and relapse-free survival. (This study did not include an
observation group as a control).

Melanoma is the most life-threatening type of skin cancer, causing nearly
8,000 deaths each year in the United States alone. High-risk patients
have a 50 to 80 percent chance of disease recurrence without adjuvant
treatment, or additional treatment after surgery, according to Dr.
Kirkwood. Furthermore, once this type of cancer recurs, it is often more
difficult to treat.

This latest report on E1694 reaffirms the significant and consistent
efficacy of high-dose interferon alfa 2b, as reported from a prior study
led by Dr. Kirkwood, which led the FDA in 1995, to approve it as the
first effective adjuvant therapy for high-risk melanoma. Five years
later, interferon alfa 2b remains the only FDA-approved adjuvant therapy
for this disease.

The current study also puts to rest lingering concerns about the
effectiveness of interferon alfa 2b in terms of survival impact. These
concerns probably account for the current reluctance on the part of some
clinicians in the United States, Europe and Asia to use high-dose
interferon alfa 2b in appropriate high-risk settings, according to Dr.
Kirkwood.

Run from 1996 to 1999, the ECOG-Intergroup trial E1694 involved 880
surgically treated, high-risk melanoma patients who had primary tumors
that were greater than 4mm in depth or who had melanomas that had spread
to nearby lymph nodes. Patients were randomized to receive either a
course of interferon alfa 2b (20 MIU/m2 administered by IV infusion five
days per week for 4 weeks, followed by 10MIU/m2 administered
subcutaneously three times per week for 48 weeks) or to receive the GMK
vaccine (given weekly for one month and then at three-month intervals for
two years).

Interferon alfa 2b is a recombinant version of naturally occurring
leukocyte (white cell) alfa interferon, which has been shown to exert
both antiviral and immunomodulatory effects. Schering-Plough Corporation
(Kenilworth, N.J.) markets interferon alfa 2b (INTRON A®) for 16 major
antiviral and anticancer indications worldwide. A major concern with
interferon alfa 2b use has been that most patients experience flu-like
side effects, such as muscle pains, headache, fever and chills, over the
course of therapy, and they may also show reduced white blood cells.

The comparison vaccine used in E1694, GMK, contains an antigen called
GM2, which has been shown to stimulate the immune system to produce
antibodies against this marker of melanoma. Melanoma patients with
anti-GM2 antibodies have a better outcome than those who do not have
anti-GM2 antibodies. This has been shown in multiple studies, including
one early randomized, controlled clinical trial that demonstrated a trend
to improved relapse-free survival in patients treated with a GM2 vaccine.
GMK is manufactured by Progenics, Inc.

E1694 was closed in April 2000, when an interim data analysis showed
compelling evidence that interferon alfa 2b was significantly superior to
GMK in prolonging both overall and relapse-free survival. Dr. Kirkwood's
presentation in Hamburg provides the full, final analysis of this overall
survival and relapse-free survival impact. At two years, the evidence
reveals that deaths and relapses were reduced by 33 percent in patients
receiving interferon alfa 2b.

Interferon alfa 2b is the first, and to date, the only adjuvant therapy
indicated for high-risk patients with melanoma that has been completely
treated with surgery. It won FDA approval in 1995 on the basis of a
clinical trial (ECOG's E1684 study) showing that this immunobiological
therapy improved overall survival and relapse-free survival in high-risk
patients. The study compared high-dose interferon alfa 2b (20MIU/m2) to
observation in a similar population of patients, and showed nearly
identical benefit in terms of both prolonging survival and in reducing
the frequency of relapse. Patients receiving high-dose interferon alfa 2b
in that initial trial had significant benefit, in terms of both overall
survival and relapse-free survival.

At the same time ECOG's E1684 study was being completed, however,
investigators led by Dr. Kirkwood began a second, large-scale study
(ECOG's E1690 study) comparing high-dose interferon alfa 2b and low-dose
interferon alfa 2b, both in reference to observation. E1690 evaluated a
somewhat larger number of high-risk patients with deep primary tumors
(irrespective of whether nearby lymph nodes were cancerous). Results of
this study, published after the 1995 FDA approval of interferon alfa 2b,
showed significantly improved relapse-free survival, but they did not
confirm the overall survival benefit seen in E1684.

"We think that the overall survival benefit was not seen in E1690 because
patients initially randomized to receive no interferon alfa 2b received
the drug after relapse from the observation arm of the study. This
crossover in our study design confounded our results so that an overall
survival benefit of interferon alfa 2b could not be measured. E1694 is a
two-fold larger study, and it confirms the overall survival benefit of
high-dose interferon alfa 2b in a decisive and unequivocal manner."

Unfortunately, according to Dr. Kirkwood, the controversial outcome of
E1690 may have contributed to the hesitation of some members of the
medical community, both in the United States and in Europe, to use
high-dose interferon alfa 2b in a high-risk setting.

Although interferon alfa 2b proved superior to the GMK in the E1694
study, Dr. Kirkwood cautioned that GMK may still have therapeutic benefit
in combination with interferon alfa 2b, or with a variety of other
vaccines in the treatment of melanoma. Some of these vaccines are
designed to induce more effective T cell responses to melanoma, a goal
that is quite distinct from the goal of inducing antibody responses as
tested in E1694. In 1994 when the currently reported trial was designed,
GMK was the most promising vaccine the ECOG Melanoma Committee evaluated,
according to Dr. Kirkwood, and the data that support it remain a strong
impetus to evaluate vaccines more carefully along both antibody and T
cell lines.

The ECOG has just initiated a trial of a triple vaccine with or without
interferon alfa 2b, or a growth factor (GM-CSF) for immune cells, with
the goal of inducing better T cell responses to melanoma. The UPCI has
just initiated a novel vaccine that also targets a form of T cell that
previously has not been capable of being stimulated by vaccines, the
helper CD4 T cell. According to Dr. Kirkwood, as the preliminary results
of each of these approaches shows promise, they will be factored into the
interferon approach that now has become the foundation of new adjuvant
therapy for melanoma.

###

* Dr. Kirkwood chairs the Eastern Cooperative Oncology Group's (ECOG's)
Melanoma Committee, which is headquartered at the University of
Pittsburgh. The study reported on was done in collaboration with the
Southwest Cooperative Oncology Group and the Cancer/Leukemia Group B.

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Surgery Without a Scalpel Posted Monday, August 28, 2000 by ctustis
Technology May Change Cancer Treatment Forever

The CyberKnife uses a noninvasive radiation technique to treat cancer. It
is currently available at five hospitals in the United States.
(ABCNEWS.com)

By John Yang

S T A N F O R D, Calif, Aug. 28 - Think of cancer surgery and what
usually comes to mind are frightening images of a long, arduous procedure
with an often painful recovery period.

But a new piece of technology offers what could be a major breakthrough
in cancer treatment - no scalpel, no blood, no postoperative pain. It is
called the CyberKnife and it combines powerful radiation with pinpoint
accuracy to kill tumors.

"It changes everything about surgery," says Dr. John Adler, a
neurosurgeon at Stanford University who developed this revolutionary,
noninvasive device. "This is all done remotely, done automatically.
Although the doctor remains a critical element of the entire surgical
process, it changes the whole notion of what surgery is."

The device, which is made by Accuray, uses technology similar to what the
Pentagon devised to target cruise missiles. For the first time, digital
X-ray images target the tumor, even if the patient's head moves. Before,
surgeons would have to use a metal frame - which was actually screwed
into the patient's skull - to target the radiation. That made the
treatment impractical for many patients, especially children.

Allows More Treatment Options But the flexibility and added accuracy of
this new technology lets doctors use stronger doses of radiation,
resulting in fewer treatments and less damage to surrounding tissue.

That's what appealed to Dana Garner, who has a tumor on her hearing
nerve. Her original physician offered traditional surgery as the only
option to restoring the hearing she had lost in her right ear. But she
didn't want that.

"I didn't want him cutting into my brain," she says. "There are so many
possibilities of nerve damage."

She discovered CyberKnife while researching options on the Internet. "It
allows us to treat the tumor with an excellent chance of killing the
tumor, and/or preventing tumor growth, but minimizing the chance of
injury to the nerves that are adjacent to the tumor that control facial
movement and hearing," says Dr. Steven Chang, the Stanford Medical Center
neurosurgeon who is now treating Garner.

For some it is the only option. Valorie Degrendele had a growth in her
spinal cord - a cluster of blood veins called an arteriovenous
malformation - that surgeons could not reach. She was treated by the
CyberKnife three years ago.

"There was just no other way," she says. "They had given up on me. They
said I would be paralyzed, if not dead."

Availability Increasing In addition to Stanford Medical Center, the
technology is available at four other locations around the country: the
Cleveland Clinic in Ohio; the University of Texas Southwest Medical
Center in Dallas; the University of Pittsburgh Shadyside Hospital in
Pittsburgh; and Newport Diagnostic Center in Newport Beach, Calif. Plus,
it is used at three hospitals in Japan.

The Food and Drug Administration has cleared its use on tumors in the
head and neck. It's designed to treat cancers anywhere in the body and is
now being tested on tumors in the lung and pancreas.

"It's outpatient, it's less expensive and overall it's probably even more
effective than regular surgery for the large number of cancers that we
are treating at this point," Adler says.

For patients like Dana Garner, that means the hope that their tumors may
be eliminated more efficiently, without the fear of traditional surgery

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Newly discovered gene makes cancer spread Posted Wednesday, August 2, 2000 by ctustis
Genome project: Data sheds light on the disease's deadly migration
to new cells.

BY DELTHIA RICKS
Newsday

Using molecular data from the Human Genome Project, scientists have
identified a gene that causes some cancer cells to break away from
their original tumor and seed new tumors in distant sites.

It is a discovery scientists are hailing as a significant advance in
understanding the molecular mechanisms that underlie why cancer cells
stray.
The consequences of that wanderlust, researchers estimate, ultimately
lead to 90 percent of all cancer deaths.

The study is one of two reported in today's issue of the journal
Nature that focus on cancer's spread -- metastasis -- and malignant
melanoma, a deadly form of skin cancer that will afflict more than
40,000 Americans this year.

Putting brakes on cancer?

The findings from both investigations hold promise of using
gene-based data to stop the spread of cancer before it starts,
medical experts say. One study focuses on the role of one gene in
triggering spread of malignant melanoma. The second examines a host
of genes involved in the cancer's metastasis.
``It is the metastatic cell, not the primary one, that proves fatal
to the patient,'' said Dr. Richard O. Hynes, director of the Cancer
Research Center at the Massachusetts Institute of Technology.

Hynes and colleagues have identified the role of a gene dubbed rhoC,
a significant trigger in the spread of some forms of malignant
melanoma.

Using mouse and human cancer-cell lines, Hynes and his team were able
to elucidate how the gene triggered the cascade of events that allows
a melanoma cell to migrate and invade.

Deadly invasion

The process of metastasis has been one of medicine's enduring
mysteries. Cancer cells can evade the body's warrior cells and
proteins and establish new, deadlier cancers far afield of the mother
tumor.

Hynes said not all cancer cells are capable of breaking from the
primary tumor and burrowing through walls of tissue to reach the
bloodstream, their conduit to new sites. ``The bloodstream is
turbulent, it's a raging river,'' Hynes said.

Cells that are metastatic not only hold the keys to escape, they are
hardy enough to survive the buffeting of the blood. What makes a
renegade cancer cell a survivor, Hynes said, is part of its mystery.
It maintains its properties of adhesion, the biological glue that
keeps all cells in their places, long enough to grow and divide in
the original tumor. Then it loses those properties to break away and
escape. Metastatic cells regain their adhesion properties when they
establish a new tumor elsewhere in the body.

RhoC, Hynes said, sheds new light on the processes of having, losing
and regaining adhesion, one of the more confounding abilities of a
rogue cancer cell.

Dr. Robert Radinsky, a physician-scientist at Amgen, a pharmaceutical
giant in Thousand Oaks, called the MIT discovery a ``significant
step.'' Radinsky, who for years has specialized in the study of
metastasis, first at the M.D. Anderson Cancer Center in Houston and
now with Amgen, said metastasis is the key event in cancer biology.
Without it, cancer would be an easily treatable disease.

Often too late to stop

``Metastasis is dynamic,'' Radinsky said. ``Genes are turned on and
off all of the time. It is a multi-step process. And usually by the
time a patient comes in to be diagnosed, metastatic cells are already
in distant sites.''

Meanwhile, scientists at the National Human Genome Research Institute
in Maryland have discovered a genetic ``signature'' that may help
explain even further how malignant melanoma can spread.

Together, the two studies reveal for the first time the intimate role
numerous genes play in determining which malignant cells will migrate.

``By learning about what makes each patient's tumor grow, what makes
it spread or not spread, hopefully you could tailor therapies to the
individual patient rather than use a one-size-fits-all kind of
approach,'' said Dr. Paul Meltzer, a senior investigator at the
National Human Genome Research Institute.

Using a sophisticated molecular technique called DNA micro arrays,
which are small glass slides containing tiny amounts of known genes,
the scientists could ``read'' the genetic data to determine which
genes were turned on or off in melanoma.

Computers in turn searched for hidden patterns in the genes. Because
the technique allows scientists to know which genes are being turned
on and off, it holds the promise of creating customized treatments
for patients.

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Cancer survivor plans continental ride for life Posted Tuesday, August 1, 2000 by ctustis
(Published Sunday, July 30, 2000)

By Anna Marie Lux/Gazette Staff

Elizabeth McGowan is preparing to make a journey of celebration.
This time, the 39-year-old former Janesville resident is bicycling across America.
She'll leave Astoria, Ore., on the Pacific Ocean in mid-August and pedal 4,250 miles to Yorktown, Va., on the Chesapeake Bay. If all goes well, she'll arrive on the East Coast in mid-November.
Within the first 300 miles of her journey, she'll encounter a 4,000-foot climb to Oregon's McKenzie Pass, which has several steep, narrow switchbacks. Between Lander and Rawlins, Wyo., near the Continental Divide, she'll spin her way along a tenuous, 123-mile stretch with few services.
Later, she'll make the longest ascent of her trip, about 70 miles, up and over Lolo Pass, from Idaho into Montana.

Sound hard? You bet. Super hard.

But all Elizabeth will have to do to keep going is remember the image of that nurse looking for a vein in her arm. Or think of those frightening months she can't remember during chemotherapy. Or recall the tone of her surgeon's
voice when he told her: "We don't know what we're going to find."

"This will be a walk in the park compared to that," she says.

Since she was 24, Elizabeth has been duking it out with malignant melanoma. She knew she could develop the often-deadly cancer after she watched her father die of it when she was 15. Her fears came true when she discovered a skin lesion on her upper back.

In the decade after her diagnosis, the nasty disease spread to her lymph system, right lung, gallbladder and liver.
"Numerous treatments involving immunotherapy, chemotherapy, extensive surgeries and a secret weapon--the McGowan fighting gene--kept me chugging along," Elizabeth says.

"No wonder the technician who does my regular CT scan at the hospital gasps when she sees my innards on film. I just laugh and tell her that I'm pretty much held together with staples and baling twine."

In April, Elizabeth marked five years of being cancer free when she got a thumbs up from her oncologist, Dr. Paul LeMarbre at the Waukesha Memorial Hospital Regional Cancer Center in Waukesha.

Now she feels compelled to tell people that she's still alive.
"And I'm grateful for it."

She could continue as usual with her sweet life as a caretaker with her partner, Don Looney, at the Lulu Lake preserve. The Nature Conservancy property for plants and animals, just over the Walworth County line, is one of southeastern Wisconsin's most pristine natural areas.

But not Elizabeth.

She believes too much in giving back all she can to make her part of the universe a better place. She'd never get too comfortable because then, as she explains, she'd be in danger of flatlining.

And Elizabeth knows that life, every minute, every day, is far too precious for complacency.

So last spring, as she listened to frogs in a stirring lowland, the details came together in her head. She had been thinking about a cross-country bike trip for some time. But she wanted it to be more than just a ride across America.

"People still think that cancer is a death sentence. I want to show them that you can survive cancer. I've come through this experience, and I am a better person for it," she says.

So along the way, as Elizabeth pedals through the little towns that spread across our nation's midsection, she will talk to people. She doesn't ever want to sound preachy, but she will tell them that melanoma is becoming more
prevalent worldwide, and she will caution them to use their sunscreen. She also will give ample encouragement and hope to those in need.

But that's not all.

She has christened her trek "Heals on Wheels" and turned it into a fund-raiser for the Waukesha Memorial Hospital Regional Cancer Center.

"I'm eternally grateful to Dr. LeMarbre there, who helped me go through this step by step, giving me real hope and the belief that I could come through this," Elizabeth says. "And to the other professionals who were instrumental in
keeping me alive."

All the money she raises will be donated to the cancer center, and the hospital foundation has agreed to be a clearinghouse for all the corporate and individual donations she receives.

Elizabeth is paying for all the bicycling, gear and travel with her own money.
When she first called Kay Ruekert, development officer for the Waukesha Memorial Hospital Foundation, with the idea of a cross-country bike trip, Kay responded: "Oh my goodness!"

"I'm very impressed with Elizabeth," Kay says. "Not only will she be raising money for cancer research and education, but she will also be saving lives. People will listen to her when she talks to them. She will serve as an inspiration."

Elizabeth has long been a good communicator. In fact, she's made a living from it. Maybe you remember when she worked as a reporter at The Janesville Gazette from December 1987 until early 1991.

During that time, the cancer recurred in her lungs, and she underwent chemotherapy on weekends, while continuing to write.

After the tumors shrank, she took a weeklong bicycle ride around Wyoming in spring 1990. The next year, she walked the Appalachian Trail for six months to decide what direction she wanted her life to take. From its start in Georgia to its finish in Maine, she hiked all 2,167 miles--through 14 states, eight national forests and six national parks.

Along the way, she met hiker Don Looney of South Carolina. He not only turned out to be a welcome hiking partner but a treasured life partner. They married in 1997.

While cancer has wreaked havoc on some parts of Elizabeth's life, it has given her direction.
"It's made me more appreciative of things around me. It also makes me not want to waste a minute. My motto is: 'If not now, when?'"

Along the way, she hasn't given up her dreams, but cancer has caused her to adjust them.

"Everyone has some albatross that they carry. I've always felt that I have to keep moving and staying involved because if I slowed down the cancer would pin me down and take me over. I've always lived an accelerated life."

She never thought about reaching age 40--until now.

"This is a real sweet time, but who knows if it will last," she says.

Elizabeth knows that not every day on the road will be a picnic.

"But I only have to get over those mountains once."

She will travel alone on a Trek 7200 hybrid bicycle. She will carry a sleeping bag, a tent, a tarp and a few essential clothes. She's still debating the rest of her gear.

Elizabeth's journey will take her through 10 states, including Kansas and Missouri in the heartland. She will use maps from Adventure Cycling, a group based in Missoula, Mont., which first charted the TransAmerica Trail in 1976.

In some places, friends will join her for a short while. In Illinois, she will meet up with Don, who will be her lifeline to home.

At first, she will be kind to her body and start out slowly. Later, she wants to pedal up to 60 to 70 miles a day.

Her legs are sturdy, but she says it takes more than strength to make such a long, strenuous journey. "It takes will. It becomes a mental game. I have to keep reminding myself when I'm out there that there will be a downhill."

She keeps in mind, too, how much fun biking is.

"It's exhilarating to fly down those hills and to pretend that you're 7 years old again. Believe me. This isn't a chore that I'm taking on," Elizabeth says.

"This is a celebration of life."

To donate, write your check to Waukesha Memorial Hospital Foundation and mail it to: "Heals on Wheels," Waukesha Memorial Hospital Foundation, 725 American Ave., Waukesha, Wis., 53188.

People can track Elizabeth's cross-country progress by logging on to the hospital's Web site at
www.waukeshamemorial.org. Elizabeth's e-mail is:
herron@netwurx.net.

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Canada researchers make major anti-cancer discovery Posted Friday, June 30, 2000 by ctustis
By David Ljunggren

OTTAWA (Reuters) - Canadian researchers said Wednesday they had made a potentially significant breakthrough in the fight against cancer by discovering that tumor cells could be killed by injecting them with a rare virus.

Dr John Bell of the University of Ottawa said his team had found many common cancers were destroyed by Vesicular Stomatitis Virus (VSV), which is not infectious in humans.

"We're excited. We think this is an important step forward," he told Reuters in an interview. In laboratory tests the new treatment killed
cells from melanomas and leukemia as well as lung, breast and prostate cancers.

Bell said 15 years of research into tumors had shown that many cancer cells suffered from a genetic flaw that made them vulnerable to VSV, which has been under study for the last 50 years or so.

"Knowing what this (genetic) defect was and knowing the properties of the virus, we thought this would be a good fit. So we then tested the
virus and sure enough it was very effective," said Bell.

More tests will now be carried out on laboratory animals and if all goes well the first clinical trials on human beings could start in about 18 months.

"Dr Bell's findings are potentially very important. We look forward to seeing the results of the preclinical studies to evaluate the possible
efficacy of this virus as a cancer therapy," said Robert Phillips, head of Canada's National Cancer Institute.

Cancer is the second biggest killer in most developed countries after heart disease. In 1997 the World Health Organization said 10 million
people were diagnosed a year with the disease and six million died.

"There are other people out there in Canada, the United States and Europe who are working on viruses as well and we think probably their
viruses are working the same way that ours is and they haven't appreciated it yet," said Bell.

The team experimented on human melanoma cells which had been transplanted on to mice and also worked on other kinds of human
cancer cells grown in laboratories. The findings will be published in the July 1 edition of Nature Medicine magazine.

The one possible cloud on the horizon is how human patients react to the large amounts of VSV that Bell's team said would have to be
administered for the treatment to be effective.

"We have to do some more work to convince ourselves this wouldn't be toxic to humans. We don't think it will be but we have to be absolutely sure," he said.

"Right now, everything we have suggests to us that normal humans would not be affected by the virus, since mice are not but human tumors are. That's why we're fairly optimistic."

Another problem is making enough pharmaceutical-grade VSV for the trials and the University of Ottawa has signed a deal with Maryland-based Pro-Virus Inc. to ensure a steady supply.

"Whether it's the virus or the defect or the combination we've discovered we think this will have important implications in developing new therapies," Bell said.

"I don't think we're trying to get anyone's hopes up. I think the people out there dealing with cancer every day need to have something to be optimistic about. In their battle they need to have something on the horizon." Comments (1)

Two-Drug Combination Therapy Shows Promise Against Melanoma Posted Tuesday, June 27, 2000 by ctustis
Melanoma researchers at University of California, San Diego (UCSD) have
developed a new drug-combination therapy that has proven in Phase II clinical trials to be significantly better at extending patients’ lives than any other drug therapy.

The two drugs, tamoxifen and cisplatin, are commonly used chemotherapeutic agents. Interestingly, neither drug, when used alone, has proven effective against melanoma.

“For reasons that aren’t yet clear, this combination creates a synergism that is highly toxic to melanoma cells,” said Edward F. McClay, M.D., principal investigator of the study and director of the Melanoma Care Unit at UCSD Cancer Center.

Results of the clinical trial are being published in the July 2000 issue of the British Journal of Cancer. The clinical trial was based upon earlier laboratory work in which McClay and colleagues first identified this synergistic interaction.

“If diagnosed and treated early, melanoma is highly curable,” said McClay, professor of medicine at UCSD School of Medicine and a respected national authority on melanoma. “Unfortunately, melanoma is often diagnosed when it’s more advanced and the chances of recurrence are quite high. If it recurs, it often does so with a much more aggressive and lethal personality.”

In this study, the researchers treated 153 patients who were at high risk for recurrence or who had already had a recurrence. Participants received tamoxifen for seven days with the addition of a single dose of cisplatin on the second day; they underwent the weeklong therapy each month for four months. The principal side effect was nausea. With a median follow-up period in this study of 36 months, the researchers can predict with confidence that 79 percent of participants will be alive five years after treatment. Of equal importance, 62 percent of the patients will not have had a tumor recurrence during the five years.

“These statistics, while preliminary, are very encouraging because we have had precious little to offer patients with metastatic melanoma,” said McClay. “With the best currently available treatment, the five-year survival rate in similar patients is only about 35 to 45 percent.”

Because this study was a non-randomized Phase II trial, the researchers stress the importance of next conducting a national multi-site randomized study.

Malignant melanoma is one of the most virulent and deadly types of cancer. This year, at least 48,000 new cases of melanoma will be diagnosed in the United States and 7,700 people will die of the disease. In San Diego there will be approximately 250 new case

This work was supported in part by a grant from the National Cancer Institute and by the Bruce Brunner Gorder Memorial Melanoma Fund. Co-authors are Mary Eileen T. McClay of UCSD Cancer Center; and Linda Monroe, Paul L. Baron, David J. Cole, Paul H. O’Brien, John S. Metcalf and John C. Maize, all of the Hollings Cancer Center of the Medical University of South Carolina, in Charleston, S.C.

The Melanoma Care Unit is a patient-care and research program of UCSD
Cancer Center, the only cancer center in San Diego and Imperial counties designated for both research and clinical care by the National Cancer Institute.

For information about melanoma clinical trials at UCSD, call (858) 657-8705; for trials at institutions throughout the U.S., call the National Cancer Institute’s Cancer Information Service at 1-800-4-CANCER.

Editor's Note: The original news release can be found at
http://health.ucsd.edu/news/2000_06_20_Melanoma.html



Note: This story has been adapted from a news release issued by University Of California, San Diego School Of Medicine for journalists and other members of the public. If you wish to quote from any part of this story, please credit University Of California, San Diego School Of Medicine as the original source. You may also wish to include the following link in any citation:
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CANCER SURVIVOR READY TO BE MOM Posted Thursday, June 8, 2000 by ctustis
CANCER SURVIVOR READY TO BE MOM
DIAGNOSED WITH MELANOMA, SALLY HORVATH PUT HER PLANS TO START A FAMILY ON HOLD. THREE YEARS LATER, SHE'S EXPECTING TWINS.

By Laura Zahn Pohl
Special to the Tribune
June 8, 2000

At age 30, Sally Horvath of Naperville expected to be starting a family. Instead, she found herself starting treatments for Stage III melanoma. Three years later, she is back to her original plan of starting a family, only now she is expecting twin boys in July.

"Every doctor I went to for treatment, I always asked, `Can we still have children?'" Horvath said. "Anyone who knows me knows that I've wanted a family my entire life."

The Horvaths' plans for children were interrupted when Sally found an innocent-looking mole on her chest. She didn't think much about it then, nor after a dermatologist removed it. Even when he called 10 days later, she wasn't overly worried.

"He said it was malignant," Horvath said. "The next step was to go to a plastic surgeon to make sure they'd gotten all the cancer."

Horvath still wasn't concerned, although she thought it was odd when her employer, Tom Heimsoth, called her into his office for a serious chat. Coincidentally, Heimsoth had fought melanoma seven years earlier.

He told Horvath to consult with an oncologist about her condition. "Just to please Tom, I called the oncologist," Horvath said.


It's a decision that probably saved her life. Using an advanced diagnosis technique, the oncologist found microscopic cancer cells on three of Horvath's lymph nodes. Suddenly, Horvath was dealing with Stage III melanoma, a disease that has a 40 percent mortality rate in the first two years after diagnosis.

"I have no idea how it would have manifested itself. It could have spread to the liver or lungs," she said.

Horvath underwent surgery and thoroughly researched treatment options. She received interferon treatments at the Edward Cancer Center in Naperville. She also participated in a clinical study of a vaccine at the University of Wisconsin, which required regular trips to Madison. Such treatments fight the cancer on two fronts, boosting the body's immune system and acting directly against the cancer cells.


The interferon treatments lasted a year, and so did the misery of the symptoms.


"I'd get my injections after work on Mondays, Wednesdays and Fridays, and by 9 at night, I'd feel like I was coming down with the flu," Horvath said.

Tuesdays, Thursdays and Saturdays were spent on the couch, recovering. A year ago this weekend, Horvath participated in the annual Relay for Life at Naperville North High School. She had reached the all-important two-year milestone, and as she walked to raise funds for the American Cancer Society, she talked with nurses from the cancer center about having a family.

She eventually got the go-ahead from Dr. Alex Hantel, her doctor at the center. She and her husband, Dave, also had some serious discussions about what to do.

"It's a lot to think about--the cancer could come back," Horvath said. "But in the end, it wasn't a hard decision. We didn't want to wait until we were 50 and say, `Gee, we should've had that family we wanted to start.'"

Once pregnant, Horvath found that the usual fatigue and morning sickness were minor compared to the side effects of interferon. And this year, she will forgo the Relay for Life scheduled for Friday and Saturday and instead attend Cancer Survivors' Day on Sunday. The event runs from 1:30 to 5 p.m. at Central Park in Naperville.

Horvath stays in touch with nurses such as Kim Rohan, manager and clinical nurse specialist at the Edward Cancer Center.

"What's special is that as a survivor, she can still do what she wants to do, which is have these babies," Rohan said. "And those of us at the cancer center can't wait to see them."

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New 'combination therapy' improves survival for malignant melanoma patients Posted Wednesday, May 31, 2000 by ctustis
PITTSBURGH, MAY 30 -- Researchers at the University of Pittsburgh Cancer Institute announced that an immunomodulating agent, histamine dihydrochloride (Maxamine), used in combination with lower doses of interleukin-2 (IL-2), improved survival for stage-IV malignant melanoma patients compared with those treated with the same doses of IL-2 alone. The Phase III, multi-center study included 305 patients with this most deadly and serious form of skin cancer, randomized to receive either the histamine/IL-2 combination or IL-2 alone. The results of the study will be presented for the first time at the Perspectives in Melanoma meeting in Pittsburgh, June 1-2.

The combination therapy improved overall survival, increased survival rates at 12, 18 and 24 months, and improved time-to-disease-progression over treatment with IL-2 alone. Improvement in survival was statistically significant in patients having metastases of their melanoma to the liver, a patient population that historically has had a very poor prognosis.

Preliminary results also indicated that treatment with histamine dihydrochloride and IL-2 was safe and well-tolerated and had substantially less toxicity than the high-dose regimens under which IL-2 was originally approved. The tolerability of the histamine/IL-2 combination therapy allowed these advanced-stage malignant melanoma patients to take this treatment at home.

"The patients in this study represented a group with factors that are indicative of a poor prognosis for survival, including liver metastases," explained Sanjiv S. Agarwala, M.D., lead-enrolling
investigator for the study and associate medical director of the Melanoma Center at the University of Pittsburgh Cancer Institute. "This is the first well-controlled, multi-center Phase III trial to
show a significant increase in survival among patients with advanced metastatic melanoma."

Treatment of Malignant Melanoma
Malignant melanoma is one of the most rapidly increasing cancers in the world, with approximately 90,000 new cases of malignant melanoma and 15,000 deaths from the disease each year in the United States, Europe and Australia. At present, there is no effective treatment that has been proven to increase survival for advanced stage-IV melanoma.

"Treatment of stage-IV melanoma with chemotherapy, immunotherapy and combination biochemotherapy has provided varying tumor response rates without proof to date that any of these treatments prolong survival significantly," stated John M. Kirkwood, M.D., director of the Melanoma Center at the University of Pittsburgh Cancer Institute. "More effective treatments are required that can improve survival, ideally while maintaining patient quality of life."

Novel Therapeutic Approach
The therapeutic approach utilized in the study is designed to improve the immune system's ability to identify, disable and destroy malignant cells. Cytokines such as IL-2 are immunotherapeutic agents that stimulate certain of the body's immune cells, natural-killer (NK) and T cells, to detect and destroy tumor cells. Histamine dihydrochloride (Maxamine) enhances the effectiveness of cytokines by protecting these critical immune cells from immunosuppression. Because the combination helps cytokines to be more effective, lower and less toxic doses can be used effectively on an outpatient basis.

Survival Benefit, Patients with Liver Metastases
For all randomized patients entering the study with liver metastases (n=129), treatment with histamine dihydrochloride plus IL-2 resulted in a median survival of 283 days compared to 154 days for control patients treated with IL-2 alone (p=0.004 under the Log-Rank test).

Survival Benefit, All Randomized Patients
For all randomized patients entering the study (n=305), treatment with histamine dihydrochloride plus IL-2 resulted in a median survival of 272 days compared to 245 days for control patients treated with IL-2 alone (p greater than 0.05 under the Log-Rank test). Overall survival, adjusted for quality of life, was also significantly improved for patients treated with histamine dihydrochloride and IL-2 compared to IL-2 alone (p less than 0.0001 for the median quality-adjusted survival improvement). In addition, time-to-disease-progression was also significantly improved for those patients receiving histamine dihydrochloride and IL-2 (p=0.01).

Survival to 24 months occurred in a total of 25 percent of patients treated with histamine dihydrochloride and IL-2, compared with 17 percent in those treated with IL-2 alone. Published reports indicate that the 24-month survival for patients treated with high-dose IL-2 was 12 percent in prior studies.

Survival Benefit, Efficacy Evaluable Population
Patients treated at clinical centers that best followed the study protocol by treating all of their patients on average with two or more cycles of therapy were considered the "efficacy evaluable" population. For all patients in the efficacy evaluable population (n=219), treatment with histamine dihydrochloride plus IL-2 resulted in a median survival of 326 days compared to 251 days for patients treated with IL-2 alone (p=0.0336 under the Log-Rank test).

For all patients in the efficacy evaluable population who entered the study with baseline liver metastases (n=93), treatment with histamine dihydrochloride plus IL-2 resulted in a median survival of 363 days
compared to 157 days for control patients treated with IL-2 alone (p=0.0007 under the Log-Rank test).

###

CONTACT: Heather Szafranski, szafranskihl@msx.upmc.edu
Lauren Ward, wardle@msx.upmc.edu
University of Pittsburgh
(412) 624-2607
or
Ed Stevens, ed.stevens@pr-euro.com
PResence Euro RSCG
(619) 293-7100

Histamine Dihydrochloride (Maxamine) The clinical trial was sponsored by Maxim Pharmaceuticals, Inc., a San Diego-based bio-pharmaceutical company that holds the patent rights associated with the therapeutic use of histamine.

University of Pittsburgh Cancer Institute Ranked 12th in NCI funding and the only NCI-designated comprehensive cancer center in western Pennsylvania, UPCI is widely recognized as a leader in translating laboratory findings into applications of potential clinical importance and for its commitment to developing new and effective approaches to cancer prevention, diagnosis, treatment and care. For more information about UPCI, please access http://www.upci.upmc.edu or call the UPCI's Cancer Information and Referral Service toll-free at 1 (800) 247-4724. Comments (0)

Vical Presents Interim Data From Phase II Allovectin-7 Melanoma Trial At ASCO Posted Thursday, May 25, 2000 by ctustis
NEW ORLEANS (BW HealthWire) - Dr. M. Atkins (Beth Israel Deaconess Medical Center, Boston), on behalf of the 43 clinical centers working with Vical Incorporated (NASDAQ:VICL), presented interim safety and efficacy data from the company's ongoing Phase II Allovectin-7 registration trial for patients with late-stage metastatic melanoma at the annual meeting of the American Society of Clinical Oncology (ASCO).

The company reported that interim data are now available for the first 52 patients of about 70 planned patients. The conclusions based on these data were that the response rate and median duration of response to date confirm the activity of Allovectin-7 in the exposed patient population, and that the safety profile of Allovectin-7 remains favorable.

Treatment with Allovectin-7 resulted in a reduction in total tumor burden of 50 percent or more in 10 percent of the patients (objective clinical responses) with a current median duration of response exceeding 5 months. An additional 15 percent of the patients have stable disease, some with reductions in total tumor burden that are significant but did not reach 50 percent at this time. These are patients who have failed other treatments. Most side effects of the administration of Allovectin-7 were mild or moderate.

Deirdre Y. Gillespie, M.D., Vical's Chief Operating Officer, said, "We are encouraged that we are already seeing objective clinical responses in some patients and measurable activity in others while we are still recruiting and treating patients in this trial. There is currently no effective treatment for patients with advanced metastatic melanoma."

These data supported the previously reported recent recommendation by an independent Drug Safety Review Board (DSRB) that the Phase II trial should progress to completion. The DSRB also recommended continuation of a randomized, controlled Phase III registration trial with Allovectin-7 in patients with metastatic melanoma. At this time, too few patients have completed their treatment to analyze potential efficacy in this trial.

Allovectin-7

Allovectin-7 is a DNA/lipid complex containing the human gene encoding the HLA-B7 antigen. Allovectin-7 is designed to be injected directly into a tumor, where malignant cells absorb it and express the HLA-B7 antigen. This antigen alerts the immune system to the presence of
foreign tissue, inducing the type of powerful immune response seen in organ transplant rejection. In addition, the treatment may trigger an
immune response against additional tumor cells, both locally and systemically, by enabling the immune system to recognize other features of the tumor cells. Allovectin-7 is currently in advanced clinical testing for patients with metastatic melanoma.

Allovectin-7 Registration Trials in Melanoma Patients

Vical is conducting two separate clinical trials in patients with advanced melanoma, either or both of which could lead to registration for their respective patient populations if endpoints are achieved.

Expanded Phase II Clinical Trial

The open-label, multi-center Phase II trial is designed to confirm the efficacy of Allovectin-7 in the defined patient population which appeared to benefit most in earlier Phase II trials. Enrollment is open to patients with metastatic (spread beyond the initial site), refractory (unresponsive to standard therapy), stage III or IV disease that has not yet spread to multiple internal organs. Up to 70 advanced melanoma patients are being enrolled at leading cancer treatment centers throughout the United States. The objective is a clinical partial or complete response in at least 15 percent of the evaluable patients, persisting with a median duration of at least four months.

Phase III Clinical Trial

The open-label, multi-center, randomized, controlled Phase III trial is designed to determine the efficacy of Allovectin-7 when combined with
standard chemotherapy in patients with unresectable, metastatic melanoma not previously treated with chemotherapy. In prior trials,
Allovectin-7 was used only after standard therapies had failed. In the new trial, patients may be enrolled upon diagnosis or upon progression to stage III or stage IV disease when surgery or radiation therapy are usually no longer curative. Because Allovectin-7 is intended to trigger an immune response against tumor cells, the company believes the treatment may be more effective in patients whose immune systems have not been compromised.

Approximately 140 patients per group, randomized by sex, age, and extent of disease spread, are being enrolled into a chemotherapy-plus-Allovectin-7 experimental group or a chemotherapy-only control group. The objective is a greater relative clinical benefit for the experimental group than for the control group. Acceptable endpoints are either a significant improvement of the median time to disease
progression with no decrease in the rate of objective clinical responses, or an improvement of at least 15 percent in the rate of objective clinical responses with no decrease in the median time to disease progression.

Metastatic Melanoma

Melanoma is a skin cancer found predominantly in Caucasians, particularly in fair-skinned individuals who have experienced repeated
sunburn. According to American Cancer Society statistics, 47,700 new cases of melanoma will be diagnosed in the U.S. and 7,700 patients will
die from this disease in 2000. The National Cancer Institute estimates that about 480,000 Americans currently suffer from malignant melanoma.

If detected when the disease is still limited to one site, known as stage I and II, melanoma usually can be treated successfully by surgery. If untreated, the disease frequently spreads to the lymph glands, lungs, liver, brain and other organs. Stage III is defined as metastatic disease limited to one region and is treated with a combination of surgery and chemotherapy. Stage IV disease involves advanced regional or any distant tumors and treatment normally includes some combination of chemotherapy, radiotherapy, and surgery.

The five-year survival of patients with stage III and stage IV disease is 59 percent and 12 percent, respectively. In patients whose disease
continues to progress after they have received all available treatments, the average survival is seven to nine months.

Vical Incorporated, The Naked DNA Company(TM), is focused on the development of pharmaceutical product candidates based on its
patented gene delivery technology. A number of therapeutic and vaccine product candidates are currently under development for the prevention
or treatment of cancer, infectious diseases and metabolic disorders by Vical and its collaborative partners, including Merck, Pfizer, Aventis
Pasteur, Aventis Pharma, Centocor, Human Genome Sciences, Merial and Boston Scientific. Allovectin-7, which uses a lipid-DNA complex to
help the immune system recognize and attack cancer cells, is in Phase II and Phase III testing in certain patients with metastatic melanoma and in Phase II testing in patients with head and neck cancer. Leuvectin, which uses a lipid-DNA complex to stimulate an immune response against cancer cells, is in Phase II testing in patients with kidney cancer and prostate cancer. Vaxid, a naked DNA vaccine to prevent relapse of B-cell lymphoma, is in Phase I/II testing. In collaboration with the National Cancer Institute, a naked DNA vaccine to treat metastatic melanoma is in Phase I/II testing.

This press release contains forward-looking statements that are subject to risks and uncertainties that could cause actual results to differ
materially from those set forth in the forward-looking statements, including whether any product candidates will be shown to be safe and
efficacious in clinical trials, the timing of clinical trials, whether Vical will seek or gain approval to market any product candidates, and
additional risks set forth in the company's filings with the Securities and Exchange Commission. Actual results may differ materially from
those projected. These forward-looking statements represent the company's judgment as of the date of this release. The company disclaims, however, any intent or obligation to update these forward-looking statements.

For news releases and other information about the company, visit the Vical web site at www.vical.com.

Contact: Vical Inc. Alan R. Engbring, 858/646-1127

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American Academy of Dermatology -- Children at Risk: Protecting OurChildren From Skin Cancer Posted Wednesday, April 26, 2000 by ctustis
NEW YORK, April 26 /PRNewswire/ -- Picnics, baseball games, and
days at the beach are common recreational activities that many
families enjoy during the summer. But are parents taking the
appropriate actions during these activities to protect their children
from melanoma, the most deadly form of skin cancer? According to a
recent survey of the summertime sun protection used by adults for
their children, many parents are not effectively protecting their
children from the harmful rays of the sun, and therefore, may be
increasing their children's risk of developing melanoma during their
lifetime.

Speaking today at the American Academy of Dermatology's
Melanoma/Skin Cancer Detection and Prevention Month Press Conference,
dermatologist June K. Robinson, M.D., Professor of Medicine
(Dermatology) and Pathology, Loyola University Medical Center,
Maywood, Ill., addressed the survey results which suggest promising,
yet inadequate, efforts by parents to protect their children from the
sun. These results will be published in the May issue of the Journal
of the American Academy of Dermatology.

"Most people know that the sun is dangerous, but that does not
always translate into recognizable protective actions," stated Dr.
Robinson. "Parents need to take the warning about the dangers of the
sun seriously and act now to protect the future health of their
children."

Previous studies have confirmed that sun exposure is responsible
for the development of at least two-thirds of all melanomas.
Intermittent sun exposure, which is often recreational and frequently
occurs daily for prolonged periods of time, is also closely linked to
melanoma. Furthermore, it is estimated that 80 percent of a person's
lifetime sun damage occurs before the age of 18, a significant
portion of which occurs during peak sun hours and in the summer. This
combination of intense, intermittent sun exposure during the summer,
which results in a sunburn, increases a child's risk for developing
melanoma.

According to the survey, parents reported applying a sunscreen
with a sun protection factor (SPF) of 15 or higher as their most
frequent sun protection behavior (53%). Children's use of sunscreen
was significantly associated with sunny weather, family history of
skin cancer, prior history of sunburns in the child, fair skin, and
higher family income. In addition, children using sunscreen spent an
average of nearly 22 percent more time in the sun on a weekend than
children who were not using sunscreen.

"The study confirms that the children with the greatest risk to
experience sunburn are using sunscreen," stated Dr. Robinson. "But
the benefits of sunscreen are greatly reduced when the children who
are using sunscreen spend more time in the sun than those not using
sunscreen."

The survey showed that a child's sunburn was significantly
associated with the sunburn of the parent or caregiver. "Parents are
setting a bad example for their children by not using sunscreen on
themselves and not limiting their exposure during peak hours of
exposure by performing outdoor activities before 10 a.m. or after 4
p.m.," stated Dr. Robinson. "As role models, parents' actions and
attitudes can make a immense difference in their children's sun
safety behaviors."

The children in the survey still experienced sunburn even though
they used sunscreen as their primary method of sun protection.
Previous studies have shown that sunburn is often the result of
incorrect use of sunscreen. Since people frequently apply only 20
percent to 50 percent of the recommended amount of sunscreen, they
only receive 20 percent to 50 percent of the SPF.

"Underprotection due to inadequate application of sunscreen,
coupled with overexposure to the sun, partially explains the sunburns
experienced in this study by children whose parents reported using
sunscreen with an SPF of at least 15," remarked Dr. Robinson.

"Parents and children must be educated to use sunscreen as part of
an effective sun protection program," continued Dr. Robinson. The
American Academy of Dermatology recommends the following tips for
effective sunscreen use:

Wear a broad-spectrum sunscreen with a sun protection factor (SPF)
of at least 15.
Use sunscreens every day if you are going to be in the sun for more
than 20 minutes.
Apply sunscreens to dry skin 15 to 30 minutes before going outdoors.
When applying sunscreen, pay particular attention to the face, ears,
hands and arms, and generously coat the skin that is not covered by
clothing. One ounce of sunscreen, enough to fill a shot glass, is
considered the amount needed to cover the exposed areas of the
bodycompletely.
Reapply sunscreens every two hours or immediately after swimming or
strenuous activities.

"The survey's findings also reinforce the importance of using
multiple sun protection methods for maximum effectiveness," stated
Dr. Robinson. "Parents and children need to broaden their use of sun
protection beyond their current primary reliance on sunscreen."

In addition to wearing a broad-spectrum sunscreen with an SPF of
15 of higher, a comprehensive sun protection program includes
avoiding deliberate tanning with indoor or outdoor light, seeking
shade, wearing protective clothing, and limiting exposure during peak
hours. "Early initiation of these sun protection behaviors by parents
and consistent use throughout life may decrease a child's lifetime
risk of developing melanoma," stated Dr. Robinson.

The study results were determined by a random sample telephone
survey of 503 households within the continental U.S. conducted in
1997 by Leo J. Shapiro and Associates (Chicago, Ill.) in
collaboration with the AAD and the Centers for Disease Control and
Prevention.

The American Academy of Dermatology, founded in 1938, is the
largest, most influential, and most representative of all
dermatologic associations. With a membership of over 13,000
dermatologists worldwide, the Academy is committed to: advancing the
science and art of medicine and surgery related to the skin;
advocating high standards in clinical practice, education, and
research in dermatology; supporting and enhancing patient care; and
promoting a lifetime of healthier skin, hair and nails. For more
information, contact the AAD
at 1-888-462-DERM or www.aad.org .

Contact: Missy Gough, 847-240-1734, or mgough@aad.org, Karen
Klickmann, 847-240-1735, or kklickmann@aad.org, or Jennifer Gale,
847-240-1730, or
jgale@aad.org, all of American Academy of Dermatology

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Approach promising for melanoma Posted Wednesday, April 5, 2000 by ctustis
THE SYNTHETIC "antisense" molecule incorporates itself into a gene responsible for key functions of the cancer cell, essentially disabling it and preventing it from operating properly.
 "To our knowledge, this is the first demonstration of clinical response using an antisense-based therapy for solid tumors," said Dr. Burkhard Jansen, an associate professor of clinical pharmacology at the University of Vienna.
 Although the first tests of the therapy were designed simply to establish the best dose and establish safety, Jansen said one 90-year-old woman who was given the antisense compound - dubbed G3139 - has been free of disease for more than two months. In two other patients, tumors shrunk by more than half, and in another three, tumors visibly decreased.
 The average survival for the 14 patients in the study - all of whom had exhausted standard chemotherapy efforts to control the disease - is nine months, said Jansen. Typically, the advanced patients would be expected to die in less than six months, he said.
 "This is a very exciting development," said Dr. Peter Jones, director of the University of Southern California Norris Comprehensive Cancer Center in Los Angeles. "We have all been waiting for this type of use of antisense. The study is very encouraging."
 In the experimental therapy, researchers targeted the bcl-2 gene. In patients with certain cancers, including melanoma, the gene produces a chemical shield that protects tumors from chemotherapy. By not allowing the gene to function properly, anticancer drugs were able to attack the tumor.
 At a news briefing, Jansen explained that in the treatment regimen, patients are given G3139 intravenously for five days, after which they are administered dacarbazine (DTIC), a standard chemotherapy agent. In advanced melanoma, DTIC is usually no longer effective against the disease.
 The procedure is repeated each time DTIC is given, with some patients receiving 10 cycles of the drug, he said.
 Jansen said G3139 was well-tolerated, even by the 90-year-old. And researchers still have not reached a maximum dose at which toxicity is great enough to halt treatment.
 Melanoma is a deadly form of skin cancer that strikes 25,800 people in the United States a year; it is responsible for 24,000 deaths a year.
 The manufacturer of G3139, Genta Inc., of Lexington, Mass., is planning to begin a larger study of the drug with about 270 patients to be recruited in the United States, Canada and Europe.
 "What is exciting about this concept is that bcl-2 is overexpressed in a number of cancers," Jansen said. "Lymphoma, colon cancer, lung cancer and breast cancer could be potential targets for this strategy."

http://www.msnbc.com/news/390789.asp

Positive Results Obtained with Low-Dose M-Vax In Metastatic Melanoma Posted Thursday, March 16, 2000 by ctustis
KANSAS CITY, MO -- March 15, 2000 -- AVAX Technologies, Inc.
announced interim results from a low-dose Phase 2 study of M-Vax(TM),
a therapeutic cancer vaccine for post-surgical, stage III metastatic
melanoma made by modifying a patient's own tumor cells with a
molecule called a "hapten." The purpose of the study, which is
ongoing, is to evaluate M-Vax's ability to stimulate an immune
response against a patient's own tumor cells utilizing a lower
vaccine dose than previously tested. Lowering the vaccine dose
reduces the amount of tumor tissue required for manufacturing and
thereby expands the number of eligible patients.

Preliminary results from 23 patients demonstrate that 65% of the
patients responded favorably to the lower dose, as measured by a
delayed type hypersensitivity test (DTH), a skin test that measures a
patient's immune response against the patient's own tumor cells. The
data obtained from this study to date show the same magnitude of
positive immunologic responses as seen after higher dose M-Vax
treatment in earlier studies. Results in these earlier studies
indicated a strong correlation between positive clinical outcomes and
M-Vax's ability to induce an immunological response against a
patient's own tumor cells. Follow-up of over 350 patients to date
continues to support this correlation.

This low-dose M-Vax study is being conducted by David Berd, M.D.,
Professor of Medicine, Thomas Jefferson University in Philadelphia,
and will involve a total of 46 patients receiving seven doses of
M-Vax over a seven-week period and given a DTH test one month after
their last weekly vaccination. Currently, 32 patients have been
enrolled, with interim data available from 23 patients.

Jeffrey M. Jonas, M.D., President and CEO of AVAX Technologies, Inc.,
stated, "The interim data gathered from this revealing study continue
to support earlier results that indicate M-Vax is successful in
stimulating a patient's immune system to attack cancer cells. More importantly, this study demonstrates that we can achieve this important immunologic response with a lower dose. This finding is especially significant since the lower dose requires only half the tumor used
in previous studies to prepare the vaccine. As a result of this key
discovery, we have modified our ongoing, multicenter, pivotal
registration trial of M-Vax to use the low-dose M-Vax regimen, which
we believe enhances our ability to treat additional patients who may
have been previously excluded from the study due to the size of their
tumor."

AVAX Technologies, Inc. specializes in the development and
commercialization of novel biotechnologies, immunotherapies and
pharmaceuticals for cancer and other life-threatening diseases using
three core technologies: autologous cell (AC) vaccines, topoisomerase
inhibitors and anti-estrogens.

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Genetic test for melanoma developed at UCSF Posted Friday, March 10, 2000 by ctustis
San Francisco - A genetic test to help pathologists identify melanoma, the most common type of skin cancer, has been developed by researchers at University of California, San Francisco, and may be available to pathology labs within a year.

The test, which detects chromosomal abnormalities that characterize cancerous skin cells, was described here, today (March 9), at the annual meeting of the International Society of Dermatopathology.

A skin mole that looks suspicious to a dermatologist is usually biopsied and examined under the microscope. But even with years of experience it's sometimes impossible to make a clear decision as to whether or not the mole is cancerous. And sadly, many melanoma cases slip through the screening process; according to some insurance carriers, these cases account for six percent of the money awarded each year in malpractice suits.

Because melanoma results when a cell's genetic machinery gets out of control, Philip LeBoit, MD, a professor of pathology at UCSF, and his colleagues began comparing chromosomes of normal skin cells with those of cancerous ones. In a test called comparative genomic hybridization, they labeled DNA from normal and cancerous cells with different fluorescent dyes, then used these to identify the changes in the cancer cell's chromosomes.

These experiments were conducted by Boris Bastian, MD, an assistant professor of dermatology, Dan Pinkel, PhD, a professor at the NCI-designated UCSF Comprehensive Cancer Center, and LeBoit.

Clear patterns have emerged in the first 100 cases that LeBoit and his colleagues have studied: 82 percent of melanoma tumors lack portions of the DNA normally found on one arm of chromosome 9, 63 percent are missing sections of chromosome 10, and 50 percent of tumors have extra DNA on chromosome 7. Cancer cells that are missing DNA have shut down certain genes on that chromosome and, similarly, extra DNA suggests that the melanoma has generated extra copies of some genes on that chromosome.

By testing suspicious looking skin cells for these abnormalities, dermatologists can be much more certain of their diagnoses, LeBoit said. "Now we have a common set of abnormalities for melanoma. And most tumors have two, three or four of them," he said.

Before pathology labs around the country can begin using the test, it needs to be simplified, LeBoit said. "It now takes a more sophisticated molecular biology lab and weeks to months of work to get an answer for a given case," he said. The experimental version of the test will be replaced by one that uses fluorescent markers to light up the aberrant
chromosomal regions in tumor cells. "This type of fluorescent test is much easier to do technically," he said.

The chromosomal tests should also help when a melanoma is discovered, by showing where the cancer stops and the normal cells begin. This will enable dermatologists to cut out only the cancerous cells and leave behind the healthy ones, LeBoit said.

Contact: Kevin Boyd
kboyd@pubaff.ucsf.edu
415-476-2557
University of California, San Francisco
Source:
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Orphan Drug Status Granted to Malignant Melanoma Treatment Posted Tuesday, February 29, 2000 by ctustis
WESTPORT, Feb 28 (Reuters Health) - The Food and Drug Administration
has granted orphan drug status to Maxamine (histamine dihydrochloride), indicated as an adjunct to cytokine therapy for treatment of metastatic
malignant melanoma, Maxim Pharmaceuticals announced Friday.

Maxamine is currently being studied in three phase III trials.
Completion of the trial for the melanoma indication is expected by June, Maxim said. The company plans to file a new drug application by mid-2000.

Maxim said that according to preliminary, single-center data from one
of the trials, the survival rate of patients treated with Maxamine plus cytokine therapy was significantly greater than that of the control group.

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Compound Reverses Sun Damage To Skin Posted Friday, February 25, 2000 by ctustis
NEW YORK (Reuters Health) - Sun worshippers may someday slather on an after-suntan lotion that repairs some of the genetic damage caused by ultraviolet (UV) light. According to researchers in Germany and the Netherlands, a compound under study that contains a DNA-repairing enzyme may allow sunburn sufferers to reverse some skin-cell mutations that can later become cancer.

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Membrane-Bound GM-CSF Tumor Cell Vaccine Protects Against Aggressive Melanoma Posted Friday, February 25, 2000 by ctustis
A new gene therapy approach for a possible cancer vaccine, which uses
tumor cells genetically modified to express a membrane form of the
cytokine granulocyte-macrophage colony-stimulating factor (GM-CSF) on
the cell surface, appears to protect against an aggressive form of melanoma in animal models. The results were recently reported at the Keystone Symposia on Cellular Immunity and Immunotherapy of Cancer in Santa Fe, New Mexico, by Soonpin Yei, MD, of The Immune Response Corp, one of the study's investigators.

GM-CSF is a naturally occurring protein that helps orchestrate immune
responses and has been shown in preclinical and clinical studies to
boost the immune system's ability to recognize and destroy tumor
cells.

"Results suggest that tumor cell-based vaccines engineered to express
mbGM-CSF on their surface, rather than secrete the cytokine, may
represent a promising approach to stimulating the immune system
against this aggressive form of melanoma," said Dr. Richard M.
Bartholomew, executive director of research operations at The Immune
Response Corp. "The data also indicate that long-lasting protective
immunity may result from this form of mbGM-CSF tumor cell vaccine,"
he said.

"Previous results of this technology showed that the mbGM-CSF cancer
vaccine could effectively lead to rejection of established tumor,"
said Dr. Bartholomew continued. "We have extended these studies to
the much more aggressive B16 melanoma animal model and have shown
that the mbGM-CSF tumor cell vaccine appears to induce protective
immunity to challenge with viable melanoma tumor cells."

The study reported at the symposia involved 3 experimental groups of
mice, which were challenged with viable tumor cells after having been
immunized with either (1) inactivated tumor cells lacking mbGM-CSF
(n=10), (2) inactivated tumor cells genetically modified to express
mbGM-CSF on the cell surface (n=10), or (3) inactivated tumor cells
engineered to secrete GM-CSF (rather than express it on the cell
surface) (n=10). Nine of 10 animals in the first group grew large
tumors and died from their disease by day 43 after tumor challenge.
In contrast, the second group of animals, which was administered the
tumor cell vaccine genetically engineered to express GM-CSF on the
cell surface, had much smaller tumors, and 70% of these animals were
still alive at day 43. Furthermore, surviving animals were also
protected against a second tumor challenge after 5 months. Finally,
more than 80% of the mice in the third group vaccinated with cancer
cells engineered to secrete GM-CSF were dead at day 43.

"Currently, we are evaluating the efficacy of combining mbGM-CSF
technology with a second patented technology for cancer vaccines,
which utilizes fibroblasts genetically engineered to secrete another
cytokine, interleukin-2 (IL-2)," said Dennis J. Carlo, PhD, president and CEO. "In collaboration with Sidney Kimmel Cancer Center, we have shown that our investigational IL-2 colon cancer vaccine appears to induce immunity in colon cancer patients. We believe that combining the two vaccine approaches may yield an even more effective vaccine capable of inducing strong immune responses to the patients' tumors."

Based on these preclinical results, the company plans to test the
mbGM-CSF technology as part of its ongoing clinical vaccine program
in development for colon, glioma, melanoma and prostate cancers.

Results of mbGM-CSF tumor cell technology were first published last
year in the Journal of Immunology (Soo Hoo, et al. 1999;162:7343-7349).

GM-CSF enhances the ability of the immune system to recognize
molecules called antigens found on the surface of the tumor cells
contained in the vaccine. The immune system can only recognize these
tumor-associated antigens when they are bound to specialized cells called "antigen presenters."
GM-CSF most likely stimulates the immune system by augmenting the
interaction between tumor-associated antigens found in the vaccine
and professional antigen presenting cells, notably dendritic cells at
the site of injection.
February 24, 2000
MedscapeWire Comments (0)

High rates of skin cancer among airline pilots Posted Friday, February 18, 2000 by ctustis
Rates of skin cancer among airline pilots are up to 10 times higher
than expected, shows research published in Occupational and
Environmental Medicine. Pilots regularly flying over five time zones
seem to be at particular risk, the research shows, suggesting that
disturbances in circadian rhythms may be implicated.
Rates and types of cancer were assessed in 458 pilots, 265 of whom
flew the national Icelandic airline across European and transAtlantic
routes. These were then compared with the rates of cancer expected to
develop in the population as a whole, gathered from data supplied by
the national cancer registry, according to age.
Rates of skin cancer (malignant melanoma) were the highest for all
types of cancers. They were 10 times higher than would be expected,
and over 15 times as high for those flying international routes. Skin
cancer was also 13 times more common among those taking longer
flights and those exposed to higher levels of radiation it was up to
28 times higher. Pilots flying over five or more time zones had a
25-fold greater risk. The additional annual radiation dose for pilots
in this study was estimated at 1 to 2 milliSieverts, lower that that
estimated for UK and US pilots and well within accepted levels of
occupational exposure.
There may be several factors involved, suggest the authors, pointing
out that lifestyle, including sunbathing, may have a role.
Nevertheless, the increased rate of skin cancer among long haul
pilots suggests that disturbances in circadian rhythms, and therefore
in melatonin, the hormone critical to regulating sleep patterns, may
have a part to play.
This article is at:
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Melanoma: Posted Tuesday, February 8, 2000 by ctustis
The dark side of the sun
By James B. Meadow
Denver Rocky Mountain News Staff Writer

It can be whisper-thin, frequently underestimated and exceptionally lethal.
This year, nearly 48,000 Americans -- and 800 Coloradans -- will be
diagnosed with melanoma, the most virulent form of skin cancer, an
affliction so dark and tenacious that oncologists have referred to it as the tumor that gives cancer a bad name.

Of the people who develop melanoma, 8,000 will die, 100 of them in
Colorado, most having succumbed to the deadly effects of the sun's
ultraviolet radiation, which can wreak havoc with the body's DNA and
cellular immune functions.

If the death toll from melanoma seems insignificant viewed against that of other cancers, consider this: Skin cancer is the most common of all cancers and the fastest-growing cancer in America. In less than 30 years, the rate of new melanomas diagnosed has doubled from 6 cases per 100,000 people to 12 per 100,000.

In Colorado, the incidence of melanomas is higher than the national
average. Colorado ranks high for a combination of factors, including the 300 days of sunshine we get a year, our elevation (for every 1,000 feet of elevation, solar radiation increases from 5 percent to 7 percent) and the fact that Coloradans spend a lot of time outdoors.

Melanoma is one of the most common cancers in people younger than 30. It is the most common tumor found in women under 30 and the second-most occurring tumor in women ages 30 to 35, trailing only breast cancer.

Not that melanoma is the only form of skin cancer. "I probably see 10 people each week with new skin cancers," Denver dermatologist Dr. Barbara Reed says. She's referring mainly to basal and squamous cell cancer, which are far more common than melanoma (which accounts for only 4 percent of all skin cancers). But even though these other cancers can be fatal, none are as terribly efficient as melanoma, which causes 79 percent of all skin cancer deaths.

"It's easily one of the deadliest forms of cancer," says Dr. Rene Gonzalez, director of the University of Colorado Health Sciences Center melanoma research clinic. "Once it starts metastasizing (spreading to other parts of the body) in a patient, the immediate survival is about nine months."
Or less. Just ask Angie Kinnaird. "One acquaintance of mine told me of a loved one who had died within six weeks of being diagnosed," says Kinnaird, a state government manager who became a lay expert in the disease after surviving two brushes with melanoma.

The first occurred in 1987 when she noticed "an innocuous mole on the back of my knee." She didn't think anything of it until, six months later, she noticed it again. This time she went to a dermatologist, who didn't think it was anything to be alarmed about. Fortunately, the doctor removed it as a precaution.

"Melanomas are known for their ability to kill with a very small, thin
tumor," says Dr. David Norris, a local dermatologist and researcher. "A
tumor of only 11/2 millimeters in thickness can kill you. That's very thin when you consider that a millimeter is one one-thousandth of a meter."

Whatever the thickness of Kinnaird's innocuous mole, it had deadly potential. "They went in and did a big excision to make sure they got everything," Kinnaird says. "The doctor was pretty confident; she told me I wouldn't have another problem with it."

And Kinnaird didn't -- for four years.

Then, in 1991, much to Kinnaird's horror, doctors discovered that before its excision, the melanoma had spread to her lymph nodes. This time she was treated with interferon as well as surgery.

Four years isn't an inordinately long time between the dawning of a
melanoma and metastasizing. "It is believed that the initiating event of a lot of melanomas is sunburn in childhood, so there might be a delay of 20 to 25 years before a tumor develops," Norris says. "You can take off a melanoma and have no evidence of a disease, and 25 years later a patient may die."

That didn't happen to Kinnaird, although she came close.

"I remember the oncologist came back after getting the pathology report and said, 'It's not time to hang the funeral drape, but we have a very serious situation here."'
For Kinnaird, the whole situation was not only disturbing but surprising. "I was in my 30s at the time, and the thought of having cancer that young was very difficult to understand," she said. "I was healthy. And I had no family history of cancer -- nothing. It was a shock.

"On the other hand, I found out I was a prime candidate for melanoma --
pale skin, red hair, blue eyes and I burn easily."

Kinnaird is right: Fair skin is fair game for a melanoma.

Melanomas form in the melanocytes, the skin cells that manufacture the
skin-coloring pigment known as melanin. Although all races have the same melanocytes, the melanin of darker-skinned people -- particularly those of African heritage -- is coarser and more efficient in absorbing light, Gonzalez said. The risk of melanoma is about 20 times higher for Caucasians than it is for blacks. Still, darker-pigmented people are not immune to it, especially on the palms of their hands and soles of their feet.
Doctors also stress that most tumors of the skin are not cancerous and
don't automatically turn into cancers. But even if they do, many skin
cancers are curable in their early stages. Even melanoma, the tumor that gives cancer a bad name.

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EntreMed, Inc. Announces FDA Allowance For Human Testing of AngiostatinProtein Posted Monday, January 31, 2000 by ctustis
Phase I Clinical Trial Site Selected Testing in Cancer Patients Begins Soon

ROCKVILLE, Md., Jan. 31 /PRNewswire/ -- EntreMed, Inc. (Nasdaq: ENMD - news) today announced that it received notification from the U.S. Food and Drug Administration (FDA) granting permission for the commencement of Phase I clinical testing of Angiostatin in humans. EntreMed's Investigational New Drug (IND) application, which contained data on Angiostatin production, preclinical safety and efficacy, was submitted to the FDA on Dec. 28th, 1999.

EntreMed, Inc. has selected Thomas Jefferson University Hospital in Philadelphia as its first Phase I clinical trial site for Angiostatin protein. Dr. Walter J. Curran, Jr., Chairman, Department of Radiation Oncology, Jefferson Medical College and Clinical Director of the Kimmel Cancer Center in Philadelphia, and Dr. Robert L. Capizzi, Chairman, Department of Medicine, Jefferson Medical College, will serve as co-investigators for the trial. As with the Phase I clinical trial of Endostatin protein, now underway at three sites, the Phase I trial of Angiostatin protein will use a dose escalation method to determine its safety profile in cancer patients. Patient enrollment is scheduled to commence this quarter upon final protocol approval from the Institutional Review Board (IRB) at Thomas Jefferson University. Further information for patients and oncologists will be available through the EntreMed web site and the Thomas Jefferson University Hospital web site when patient enrollment begins.
The EntreMed website is at http://www.entremed.com/

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Promising Results on a Universal Vaccine Immune Stimulant Posted Friday, January 28, 2000 by ctustis
January 27, 2000
Journal of Immunology/MedscapeWire
Linear carbohydrate-peptide constructs based on the 13 amino acid nonnatural pan DR epitope (PADRE) and carbohydrate B cell epitopes are potent immunogens that elicit strong antibody responses specific to the target antigen, according to data reported in the February issue of the Journal of Immunology. These data provide further support that PADRE could prove important in improving vaccines against a number of infectious diseases and cancers.

Carbohydrate antigens are important vaccine targets for a number of infectious diseases including bacteria that cause pneumonia and meningitis as well as many cancers, including breast, colon, lung, prostate, and melanoma. The primary objective of carbohydrate-based vaccines is to stimulate the large quantities of IgG antibodies that are most effective in the treatment or prevention of disease. The results of the study demonstrate that combining PADRE with carbohydrate antigens results in the stimulation of large quantities of IgG antibodies that specifically recognize the target carbohydrate.

The rest of the article at http://www.medscape.com/MedscapeWire/2000/0100/medwire.0127.promising.html Comments (0)

Cleveland Clinic treats Canadians Ontario cancer patients Posted Sunday, January 23, 2000 by ctustis
Cleveland Clinic treats Canadians Ontario cancer patients avoid overcrowded facilities with government program
Associated Press
CLEVELAND: The Cleveland Clinic has landed a contract to treat sick Canadians who otherwise might face long delays getting treatment in that country's overcrowded health care system.
The contract will pay for 6 1/2 weeks of radiation therapy, airline tickets for patients and their spouses, meals and hotels.
The contract is similar to ones the Canadian government has with Detroit and Buffalo hospitals.
`We have a shortage of radiation therapists, and the waits have become unacceptably long,'' said Kristin Jenkins, a spokeswoman for Cancer Care Ontario, an agency that oversees cancer programs.

The rest of the article at:
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Copper-lowering drug stabilizes advanced cancer in anti-angiogenesis trial Posted Friday, January 21, 2000 by ctustis
ANN ARBOR, Mich. - By depriving cancer tumors of the copper supply they need to form new blood vessels, researchers at the University of Michigan report they have stopped the growth and spread of the disease in a small group of patients with advanced cancer for over a year.

Five of six patients whose copper levels were kept at one-fifth of normal for more than 90 days had no growth of existing tumors or formation of new ones, according to a paper published in the January issue of Clinical Cancer Research. The sixth had progression of only one tumor; all other tumors within her body remained stable. Twelve other patients did not achieve the target copper level, or could not stay at the target level for 90 days, because of disease progression.

The rest of the article at:
http://www.med.umich.edu/opm/newspage/copper.htm

New Feature Posted Thursday, January 20, 2000 by ctustis
Talkback, a new feature, has been added. It will allow you to comment on the news item Comments (0)

Drug blocks opioid side effects: Could improve palliative care Posted Wednesday, January 19, 2000 by ctustis
Methylnaltrexone, a drug designed to reverse one of the most troubling problems caused by opium-based analgesics without interfering with pain relief, is rapidly effective at low doses with no apparent side effects report researchers from the University of Chicago Medical Center in the January 19, 2000, issue of JAMA.

More than 250,000 terminal cancer patients each year take opioids, such as morphine, for pain relief. About half of those patients experience severe constipation. The discomfort can be so great that many patients choose to forego the pain relief in order to avoid the constipation.

In this double-blind, placebo-controlled study, methylnaltrexone promptly reversed opioid-induced constipation. In more than 90 percent of patients, relief came within one minute of the first infusion.

"By preventing this debilitating but little-discussed problem, methylnaltrexone could substantially enhance the quality of the last months of life for terminal cancer patients and others who depend on opioid pain relievers," said the study's first author Chun-Su Yuan, M.D., Ph.D., assistant professor of anesthesia and critical care at the
University of Chicago.

"Our current challenge," notes his co-author Joseph Foss, M.D., assistant professor of anesthesia at the University of Chicago, "is to make this drug available to the patients who need it, so that they won't have to choose between inadequate pain relief and debilitating constipation."

Methylnaltrexone has been intensively studied, primarily at the University of Chicago, but with only limited support from the pharmaceutical industry.
The rest of this article is at
http://www.eurekalert.org/releases/ucmc-dbo011300.html

ACS Provides "Take Action" Page Posted Tuesday, January 18, 2000 by ctustis
The American Cancer Society provides a website to allow you to interact with your Congressional representative.
http://www2.cancer.org/advocacy/new_advo/index.cfm
Here you can send a message to your representative in Congress in support
of the Medicare Cancer Clinical Trials Coverage Act
and
Cancer Screening Coverage Act for 1999
At this site you will be able to enter your zip code, select email or snail
mail, fill in the blanks and send a message to your representatives.

LIFE AND DEATH GENE DIFFERENCE IN CANCER Posted Monday, January 17, 2000 by ctustis
LIFE AND DEATH GENE DIFFERENCE IN CANCER
One mutation means survival; the other means grimmer outcome

To see the item now, visit HealthScout at
http://www.healthscout.com/cgi-bin/WebObjects/Af?id=89607&ap=1

Welcome Posted Monday, January 17, 2000 by ctustis
Welcome to the news page. To be an interactive contributor to this news page you will need a user name and password. If you wish to contribute contact me at ctustis@mwt.net expressing that desire. Include your full name. Comments (1375)