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Aug. 15, 2001 |
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Free radical damage linked to cancer risk after age 60 SEATTLE -- Aug. 15, 2001 (cancerfacts.com) -- For the first time, scientists have identified a mechanism for age-related accumulation of DNA damage in prostate cells. The finding explains why a man's risk of prostate cancer dramatically increases around age 60.
The findings by the research team led by Dr. Donald Malins of the Pacific Northwest Research Institute are reported in today's issue of Cancer Research. The results show that damage to the cells' DNA, caused by unstable molecules called free radicals packs a molecular one-two punch.
Malins says the free radicals cause what is called mutagenic damage or oxidized lesions in the structure of the DNA that accumulates as a man ages. At the same time, an enzyme called Fapy (formamidopyrimidine), which repairs the oxidized bases declines.
"What we get is a threefold increase in mutagenic bases from about age 20 to 60 years old," Malins told cancerfacts.com in an interview. "At the same time the Fapy derivative, which is protective, is decreasing threefold creating a kind of double jeopardy that dramatically increases the prostate cancer risk."
Malins' team used a combination of high-tech tools (gas chromatography and a mass spectrometer) to measure the concentrations and the ratios of the oxidized lesions and the repaired lesions found in both the normal tissue adjacent to prostate tumors and the tumors themselves.
They also examined the DNA from prostate tissue taken from older men who had died without prostate cancer and found that the genetic damage in the men mirrored the damage found in the prostate cancer cells. When the researchers analyzed the statistical data and plotted the patterns of mutagenic damage and decline of Fapy repairs on graphs, they saw an interesting convergence of the curves.
"If you look at the ratio of these two slopes, they intersect at about age 60, which fits rather nicely with what is known about prostate cancer risk at that age," Malins says.
Malins says this is the first time a relationship has been shown that links DNA damage from free radicals with age and shows that the association with prostate cancer is more than coincidental. However, he cautions against concluding the free radicals cause prostate cancer.
"It is most likely why risk goes up dramatically around age 60 but it is not the whole story," Malins says. "We can't say free radicals cause cancer, rather the data shows that they play a role, but how extensive and how complete that role is we don't know."
The finding holds implications for both younger and older men and those with and without prostate cancer, according to Malins, who cites dietary studies showing a protective effect of fruits and vegetables, which have an abundance of antioxidants that trap free-radicals and render them harmless.
"In my opinion, if boys grew up eating foods rich in antioxidants and maintained this diet into later life, we would likely see a significant reduction in prostate cancer in the United States, which has one of the highest incidences in the world," he says.
Malins' research team is also pursuing development of a device that could quickly and accurately assess a man's prostate cancer risk in a physician's office based on the same technology used in his lab.
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