Individuals with a history of nonmelanoma skin cancer (NMSC) are at increased risk for other cancers, according to a study published in the August 26 online issue of the Journal of the National Cancer Institute.

Previous studies have documented that people who have had nonmelanoma skin cancer were at increased risk for developing melanoma, but it is less well-established whether they were also at risk for cancers that do not involve the skin.

In the current study, Anthony Alberg, Ph.D., of the Medical University of South Carolina and colleagues analyzed data from a prospective cohort study called CLUE II, which was established in Washington County, Md., in 1989. Alberg's team compared the risk of malignancies in 769 individuals who had been diagnosed with nonmelanoma skin cancer and 18,405 individuals with no history of the disease during a 16-year follow-up period.

NEW YORK, August 6, 2008 – Researchers at the NYU Cancer Institute and the Ronald O. Perelman Department of Dermatology have identified mebendazole, a drug used globally to treat parasitic infections, as a novel investigational agent for the treatment of chemotherapyterm-resistant malignant melanoma.

Because most patients with metastaticterm melanoma fail to respond to available therapies, the discovery of a viable investigational treatment with an established safety profile could address a serious unmet need in oncology. Effectively sidestepping the prohibitive costs and long lead times typically required to discover new cancer medicines, the NYU team screened a library of already approved drugs for activity against the most deadly form of skin cancer.

Salt Lake City—When people know the results of genetic tests confirming they have inherited an increased risk of developing melanoma, they follow skin cancer screening recommendations more proactively—much like those who have already been diagnosed with the potentially deadly disease, according to results of a study completed at the University of Utah's Huntsman Cancer Institute. and published in the June issue of Cancer Epidemiology, Biomarkers & Prevention.

Tests for mutations in the CDKN2A gene can reveal a reason that melanomas "run" in families. The study evaluated the intent to follow, and the actual practice of, skin cancer early detection methods by members of families that carry CDKN2A gene mutations. Study participants were drawn from a group of Utahns who participated in the original "CDKN2A gene hunt" 10 to 12 years ago. They already knew that their family history might put them at increased risk for melanoma, and they had previously received melanoma prevention and screening education.

CHICAGO, June 1 – The combination of two different biotherapies may be beneficial for patients with inoperable melanoma, according to a University of Pittsburgh Cancer Institute (UPCI) study presented at the 44th annual meeting of the American Society of Clinical Oncology (ASCO) in Chicago.

Researchers in the melanoma and skin cancer program at UPCI combined two biotherapies – treatments that stimulate the immune system to fight cancer – and found the results promising in terms of anti-tumor effects and tolerable in terms of toxicity. High-dose interferon alfa-2b, a standard treatment for metastaticterm skin cancer, and tremelimumab, an antibodyterm thought to instigate the body’s immune system to attack tumors, were combined for the first time in this phase 2 clinical trial.

(PHILADELPHIA) – Combining natural organic atoms with metal complexes, scientists at The Wistar Institute have developed a new type of enzyme inhibitor capable of blocking a biochemical pathway that plays a key role in cancer development.

Based on studies in human melanoma cells, the research paves the way for developing new ways to treat cancer by dampening the overactive enzyme activity that leads to uncontrolled tumor growth.

Details of the study, to be published in the May 16 issue of the journal ACS Chemical Biology, show how small-molecule inhibitors can be designed to target a family of signaling proteins, called phosphatidyl-inositol-3-kinases, or PI3Ks.

DURHAM, N.C. -- By targeting and disabling a protein frequently found in melanoma tumors, doctors may be able to make the cancer more vulnerable to chemotherapyterm, according to a new study by researchers in the Duke Comprehensive Cancer Center.

“We tested a compound that can weaken the tumor by targeting a protein expressed on the surface of a melanoma cell. When chemotherapy was applied to the tumor in this weakened state it was much more effective compared to conventional therapy alone,” said Douglas Tyler, M.D., a surgeon at Duke and the Durham Veterans Affairs Medical Center, and senior investigator on this study. “These results are extremely significant because they may help us better treat patients with this deadly condition.”

According to a new study from the University of Minnesota, the earliest event in the development of sun-induced skin cancer may have been identified. The researchers found that the point of entry for skin cancer in response to sun exposure is in receptor molecules, molecular "hooks" on the outer surface of cells that also pull cannabinoid compounds found in marijuana out of the bloodstream. The research appears in the May 15 issue of Cancer Research.

"The question at the core of this research was, 'Why does ultraviolet light induce skin cancer?'" said lead researcher Zigang Dong, a professor of cellular and molecular biology and director of the university's Hormel Institute, which supported the study. "The idea is to find an agent that can prevent skin cancers after exposure to the sun."

Using gene therapy, plastic surgeons have delivered cancer fighting proteins through skin flaps placed on cancerous tumors on rats with a 79 percent reduction in tumor volume, according to a study in the May issue of Plastic and Reconstructive Surgery®, the official medical journal of the American Society of Plastic Surgeons (ASPS). This new delivery technique, which has yet to be tested in humans, did not cause toxicity in the body of rats; however, administering the same anti-tumor agent intravenously in humans has previously been shown to cause liver damage.

“This new technique may allow us to reprogram skin flaps, using gene therapy, to provide a blueprint for anti-tumor agents like Interleukin-12 to be produced in the tumor to kill cancer, while avoiding adverse side effectsterm,” said Geoffrey Gurtner, MD, ASPS Member and study senior author. “In this study we took skin flaps in animal models and delivered IL-12 directly to the tumor area with tremendous success. Since skin flaps are used thousands of times each year in cancer patients, this may potentially open up an entirely new area in plastic surgery and bring the specialty, once again, to the center of medicine.”

demonstrate that therapeutic targeting of these proteins is necessary for drugs to effectively treat this deadly form of cancer.

"We have shown that when two proteins – (V600E)B-Raf and Akt3 – communicate with one another in a mole, they cooperate leading to the development of melanoma," said Gavin Robertson, lead author and associate professor of pharmacology, pathology and dermatology, and director of the Foreman Foundation Melanoma Therapeutics Program at the Penn State College of Medicine Cancer Institute. "We have also shown that effective therapies for melanoma need to target both these proteins, which essentially eliminates the tumors.”

Skin lesions that are about the size of a pencil eraser are more likely to be melanomas, a deadly form of skin cancer, than smaller moles, according to a new study led by NYU Langone Medical Center researchers.

In a new study published in the April issue of Archives of Dermatology, the NYU researchers confirm that an important warning sign of melanoma — moles that are larger than 6 millimeters, the size of a pencil eraser — is still valid. In recent years, some researchers have argued that strict adherence to this guideline may make clinicians miss smaller melanomas.

“Diameter is a reasonable guideline to pay attention to and we did not see any reason to change it,” says David Polsky, M.D., Ph.D., assistant professor of dermatology and associate director of the Pigmented Lesions Section in the Roland O. Perelman Department of Dermatology at NYU School of Medicine, who led the study.

SAN DIEGO - A restricted-calorie diet inhibited the development of precancerous growths in a two-step model of skin cancer, reducing the activation of two signaling pathways known to contribute to cancer growth and development, researchers at The University of Texas M. D. Anderson Cancer Center report today at the American Association for Cancer Research annual meeting.

An obesity-inducing diet, by contrast, activated those pathways, said first author Tricia Moore, a graduate student in M. D. Anderson's Department of Carcinogenesis.

"These results, while tested in a mouse model of skin cancer, are broadly applicable to epithelial cancers in other tissues," said senior author John DiGiovanni, Ph.D., director of the Department of Carcinogenesis and of M.D. Anderson's Science Park - Research Division in Smithville, Texas.

An unusual form of skin cancer may be a sign of an underlying syndrome that makes people more susceptible to certain other cancers, according to researchers at The Ohio State University Comprehensive Cancer Center – James Cancer Hospital and Solove Research Institute.

Some people with rare skin tumors known as sebaceous adenomas, sebaceous adenocarcinomas, and keratoacanthomas are also at greater risk for developing colon and endometrial cancer, as part of an inherited condition known as Lynch syndrome. In addition, patients with Lynch syndrome are at risk for developing these skin tumors. 

Think you won’t run into grandparents at your local tanning salon? According to new research, you just might. In fact, a recent health survey of American adults suggests that while 20 percent of 18-39 year olds visited tanning beds, as many as 10 percent of those between 50 and 64 years of age and eight percent of those older than 65 tanned indoors.

Researchers at Fox Chase Cancer Center in Philadelphia analyzed data about indoor tanning behaviors collected in 2005 as part of an annual health survey called the National Health Interview Survey (NHIS). Their findings were published online today in the Journal of the American Academy of Dermatology.

Targeting and killing the non-malignant cells that surround and support a cancer can stop tumor growth in mice, reports a research team based at the University of Chicago Medical Center in the March 1, 2008, issue of the journal Cancer Research. The discovery offers a new approach to treating cancers that are resistant to standard therapy.

Many solid tumors develop elaborate mechanisms to prevent recognition and elimination by the immune system. Due to their genetic instability they often discard the tumor antigen-presenting cell-surface structures that alert the immune system that these cells are harmful. Without these “flags,” the white blood cells fail to recognize and kill infected or cancerous cells. These tumors then often grow rapidly and resist treatment with chemotherapyterm or efforts to boost the immune system's response to the tumor.

One might call it a tale of two melanocytes. Given the same genetic mutation, why does one melanocyte shut down growth and become a relatively benign mole, while another rages out of control and develops into deadly melanoma"

In trying to tease out the answer to this simple question, Howard Hughes Medical Institute (HHMI) researchers have uncovered a protein that stops the growth of melanoma, a cancer that develops from pigment-producing cells in the skin called melanocytes. HHMI investigator Michael Green and colleagues at the University of Massachusetts Medical School reported their identification of the genetic underpinnings of a new way to thwart one of the deadliest forms of cancer in the February 8, 2008, issue of the journal Cell.