Sunbathers enjoying the summer rays can thank the body's natural sunscreen - a layer of pigmented cells - for preventing much damage to the body. In turn, those dark-colored cells themselves might be destroyed by solar radiation if they didn't contain a protective mechanism that allows them to survive.

The findings, reported in the June 14 issue of the journal Cell, may explain why tumors that arise from melanocytes (pigment-producing skin cells) are particularly resistant to chemotherapy and radiation," says David Fisher, MD, PhD, a Dana-Farber researcher. "Melanoma is one of the most difficult tumors" to try to combat with cancer therapies.

An estimated 53,600 Americans will be diagnosed with melanoma this year and 4,700 Americans will die from the disease, according to the American Cancer Society. Melanoma accounts for about only 4 percent of skin cancer cases, but it causes about 79 percent of skin cancer deaths.

Fisher is the senior author of the paper, which is featured on the cover of Cell, that describes a series of experiments that were conducted during the past several years. Gael McGill, a graduate student, and Martin Horstman, a postdoctoral fellow in the Fisher lab, are first authors. The report implicates a gene, known as MITF, in enabling both normal and malignant cells to escape apoptosis, a natural process that triggers suicide in a cell that has reached the end of its useful life cycle.

Apoptosis kicks in when a cell's DNA is damaged, assigning it to death rather than risk chaotic, dangerous reproduction by the errant cell. Many cancer drugs work by inducing cancer cells to undergo apoptosis instead of continuing to divide unchecked.

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Contact: Bill Schalaler
william_schaller@dfci.harvard.edu
617-632-5357
Dana-Farber Cancer Institute
13-Jun-2002