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As men age, prostate epithelial cells are subjected to substantial stresses, and these stresses can damage DNA, thereby causing cellular transformation. The aging prostate gland acquires numerous foci of cancer cells that arise from distinct clonal transformation events.1 That most of these foci never develop into clinically detectable cancer is consistent with the frequent finding of prostate cancer during autopsies of asymptomatic men in whom the condition was never diagnosed.2 Susceptibility to prostate cancer has a clear heritable component: men are at an increased risk for the disease if they have a first-degree relative with prostate cancer. The more relatives . . .
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Edward P. Gelmann (2008) studied this question.
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