That does not mean, however, that sunbathing poses a minimal risk of developing melanoma. Researchers say that ultraviolet A (UVA) radiation, the rays in sunlight that reach the deeper layers of skin and are associated with signs of aging, can damage the DNA in melanocytes, the pigment-producing cells that give rise to melanoma.

“Although we have refined the common wisdom that excess sun exposure is always associated with increased risk of skin cancer, the take-home message for the public is still the same – limit sun exposure and use a sunscreen that blocks both UVA and UVB rays,” says the study’s lead investigator, Qingyi Wei, M.D., Ph.D., professor in the Department of Epidemiology.

In trying to learn more about skin cancer, researchers analyzed the ability of UVB radiation to damage a cell’s chromosomes. Previous studies at M. D. Anderson have shown that melanoma patients often have a reduced capacity to repair the DNA damage from UVB exposure.

In the latest study, researchers gathered white blood cells from 469 M. D. Anderson skin cancer patients and 329 cancer-free control subjects. Of the skin cancer patients, 238 were diagnosed with melanoma and 231 were diagnosed with basal and squamous cell carcinoma. All of the cells were then exposed to excessive UVB rays.

Researchers found that nonmalignant cancers had:

Greater UVB damage – UVB radiation affects cell chromosomes more severely in patients with basal and squamous cell carcinoma than those in melanoma patients.

Higher numbers of UVB chromosome breaks – The frequency of UVB-induced chromosome breaks was higher in nonmalignant skin cancer patients than in the control group, but was the same in melanoma patients and the control group. In fact, a higher frequency of chromosomal breaks was associated with a more than twofold-increased risk for both basal cell and squamous cell carcinoma.

Squamous skin cells lie near the top of the skin’s layers, while basal skin cells lie near the bottom layers. In both cases, these cells actively reproduce. When their chromosomes are damaged by sunlight, the cells often die or form a simple kind of cancer at the surface that is nonmalignant.

Because melanoma cell chromosomes resist damage from UVB radiation, they may stay intact long enough to continually amass genetic damage from both UVA and UVB radiation. “This allows the cells to hang in there longer, potentially passing on genetic mutations to daughter cells that can result in a cancer that is not sensitive to treatment,” Wei says.

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