Prostate cancer, the second leading cause of cancer death for men in the United States, is caused by changes in several tummor suppressor genes including PTEN and p53. Up to 70 percent of men with prostate cancer have lost one copy of the PTEN gene at the time of diagnosis, and p53 is absent in a high number of patients with advanced prostate cancer.
Scientists at Memorial Sloan-Kettering Cancer Center have found an unexpected effect of the interaction of these two genes in early stage prostate cancer. In a study published in the August 4 issue of Nature, researchers found that prostate tumor growth is arrested through a biological process called cellular senescence, in which cells stop proliferating and remain alive but fail to respond to normal growth signals.
This research provides some of the first evidence that this phenomenon, normally associated with stress and/or aging, also occurs in cancer both in animal models and in humans. Researchers suggest that drugs that support p53 function could delay progression of prostate cancer in Pten-deficient prostate cancer by triggering cellular senescence.
Joanne Nicholas | EurekAlert!
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