Shedding light on skin cancer

With a lifetime risk of 20 percent among Americans, skin cancer is the most prevalent form of cancer. Exposure to UV light accounts for the majority of skin cancers. UV radiation produces cyclobutane pyrimidine dimers (CPDs), which cause carcinogenic mutations in skin cells.

Our current understanding of the mechanism implies that damage only occurs during sunlight exposure. But in the Feb. 20 issue of Science, Douglas E. Brash, Ph.D., clinical professor of therapeutic radiology, and colleagues reported a novel pathway by which UV damage to DNA can also occur in the dark. When they exposed melanin-producing melanocytes in the skin to UV radiation, the cells generated “dark” CPDs for more than three hours afterwards. When they inhibited the UV-induced reactive oxygen and nitrogen species, CPD production after exposure was suppressed. Additional experiments suggested that UV-induced reactive radicals combine to excite an electron in melanin fragments, producing “dark” CPDs.

The finding “implies that UV-induced DNA damage continues even after the exposure to UV rays has ended, [which] has important implications for melanoma formation,” says Sanjay Premi, Ph.D., associate research scientist in therapeutic radiology and lead author of the study.


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