TUESDAY, Feb. 4, 2003 (HealthDayNews) -- Doctors have long known that getting a severe sunburn when you're young increases your risk of skin cancer later in life.
Now, researchers from Harvard's Dana-Farber Cancer Institute say they may finally know why.
In a study that appears in this week's Proceedings of the National Academy of Sciences, the researchers used newborn mice to illustrate how the sun's rays damage something called the Rb pathway -- a chain of biochemical signals that regulate cell activity, including suppressing the growth of malignant tumor cells.
"I think the key finding of our study is the observation of Rb pathway being hit specifically by UV [ultraviolet rays] and the potential implication of this," says study author Dr. Lynda Chin, an assistant professor of dermatology at Harvard Medical School.
Essentially, a tumor develops when normal cells experience environmental or other types of damage, causing them to reproduce at an alarming rate. Under normal conditions, Chin says the Rb pathway will sense something is not right within the cell and turn off its ability to clone itself. This, in turn, stops tumor formation.
However, if the Rb pathway becomes damaged by UV rays, particularly before the age of 17, researchers say the pathway's tumor-suppressing powers are compromised. With each new environmental assault, including sun exposure, the chances of malignant cells developing increases.
What's more, Chin says, damage to the Rb pathway appears to be a direct link to melanoma, the deadliest form of skin cancer.
"Rb pathway is presumably constraining growth of to-be melanoma cells; the UV inactivates this [protection] to allow melanoma to develop," Chin explains.
If not treated early, melanoma is among the most aggressive cancers and rapidly spreads to cells throughout the body. According to the American Cancer Society, nearly 8,000 people are expected to die of melanoma in 2003 -- a 44 percent increase since 1973.
However, if caught early, those damaged cells can be surgically removed, halting the spread of disease and dramatically decreasing the risk of death, experts say.
For dermatologist Dr. Ted Daly, the new research represents a departure from the way in which doctors previously viewed the sun's role in skin cancer.
"The accepted dogma was that the solar radiation hits a gene spot and causes kind of like a break in a zipper, so the cell no longer can divide correctly," says Daly, director of Pediatric Dermatology at Nassau University Medical Center. The new theory points up an entirely different path of destruction that, while hopeful, remains to be proven in humans, he adds.
"The negative is that mice are not men, so there's still a long way to go," Daly says.
Researchers arrived at their conclusions studying newborns of two strains of genetically engineered mice -- both bred to be susceptible to cancer. The mice then experienced various stages of cell damage, including some who received UV damage to the Rb pathway. Ultimately, the incidence of tumor growth in all the mice was compared.
What they found: The mice with the damaged Rb pathway were the ones most likely to develop melanoma. They also developed twice as many tumors, and their lesions appeared up to six weeks sooner than mice that experienced other types of cell damage.
If Chin's theory proves true in humans, she says doctors can use the Rb pathway as a guide to help distinguish between cancerous and non-cancerous skin lesions -- without the need for surgery.
That could be the most significant part of the new research, Daly says.
"You could take a biopsy, look for the Rb pathway and if it was inactivated -- indicating early UV damage -- you would know it's a typical lesion that should be removed," he says. If it worked, Daly adds, it would be "more than wonderful; it would be miraculous."
More information
Learn more about the risks for melanoma skin cancer at The Skin Cancer Foundation.
For more information on saving your skin from sun damage, visit The American Academy of Family Physicians.
