Cancer researchers have known that the tumor-suppressor gene p53 is critical in preventing cells from dividing inappropriately and becoming tumors. But now, researchers at Fox Chase Cancer Center have established that the ability of the p53 gene to perform its job depends on the type of p53 within each cell. This and another new finding about p53, published in Nature Genetics (Feb. 3, 2003 online version, March 2003 print version), have implications for tailoring chemotherapy, designing new cancer treatments, and understanding how to treat cancer in certain populations.
“The existence of two variants, or polymorphisms, of p53 isn’t new, but we’ve discovered that the variant type in each cell can influence its tumor-suppressor ability,” explains senior author Maureen Murphy, Ph.D., a molecular biologist in the pharmacology department of Fox Chase Cancer Center, Philadelphia, Pa.
When functioning properly, p53 polices cells for problems such as errant cellular growth, the hallmark of human cancer. If such harmful factors are present, p53 triggers the process of programmed cell death (known as apoptosis)-in effect, causing the “bad” cells to self-destruct. Alterations, or mutations, in this gene have been found in more than 60 percent of human cancers.
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