The Skin Cancer Foundation Journal

MAY 2013

The 2012 edition of The Skin Cancer Foundation Journal features medically reviewed, reader-friendly articles such as tanning, the increasing incidence of skin cancer diagnoses among young women, & the prevalence of melanoma among white males over 50.

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A Breakthrough In Melanoma Genetics In early 2013, researchers at Harvard and MIT announced an important new discovery. After studying 25 melanoma patients' genetic information, they found that one specifc gene, PREX2, was damaged and mutated in 11 of the patients' genomes. The researchers also observed that the amount of mutations in this gene was directly linked to chronic ultraviolet (UV) radiation exposure: the more exposure patients had, the more errors they had in PREX2, apparently confirming the role of sun damage in melanoma development. PREX2 mutations previously had been found to speed up tumor development in human THE PROMISE OF ABRAXANE In a recent Phase 3 study of 529 late-stage melanoma patients, a new chemotherapy drug called Abraxane halted the disease's advance for a median of 4.8 months, almost twice as long as the median progressionfree survival for patients taking dacarbazine, the most widely used chemotherapy (2.5 months). Overall median survival was also more than two months longer among patients taking Abraxane (12.8 months) than among those taking dacarbazine (10.7 months), though further study must be done to confrm survival benefts. Abraxane is a form of the older chemotherapy drug paclitaxel, combined with the human protein albumin. It is already FDA-approved to treat breast cancer and non-small cell lung cancer, and with its successful phase 3 results may now be submitted to the FDA for approval as a melanoma chemotherapy. Dacarbazine, approved by the FDA in 1975, is still the only chemotherapy approved for melanoma. Abraxane would be the frst melanoma chemotherapy approved in 37 years. melanocytes (the pigment cells where melanomas develop). PREX2 normally interacts with a certain tumor-suppressing protein, but UV damage may cause changes in PREX2 that allow the protein to turn from a tumor suppressor into a tumor promoter, thereby leading to melanoma. "We still can't say we know exactly how it works," says Levi A. Garraway, MD, PhD, senior coauthor of the study. "But PREX2 may be a very new category of mutated cancer genes that point us to at least one and maybe more pathways worth targeting therapeutically in melanoma." Tanning Machines Are Twice as Dangerous As the Midday Mediterranean Sun In their recent research into the dangers of ultraviolet (UV) tanning, British investigators didn't just crunch numbers. They also compared the "controlled dose" of UV radiation emitted by tanning machines with the intense midday Mediterranean sun — and refuted tanning salon operators' claims about the so-called "safety" of indoor tanning. The researchers found that that the average indoor tanning machine in England is 2.3 2.3X times more cancer-causing than the midday Mediterranean sun, and some tanning machines are up to six times as dangerous. A 2003 study suggests that US tanning beds are about as dangerous as their English counterparts. Researchers determined that nine out of 10 tanning beds in England emit more UV radiation than recommended by British and European safety standards, typically almost double the recommended amount. These excessive levels are especially worrisome considering that any UV tanning causes DNA damage that ages the skin and can ultimately cause skin cancers. The researchers found that that the average indoor tanning machine in England is 2.3 times more cancer-causing than the midday Mediterranean sun, and some tanning machines are up to six times as dangerous. 9

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