PHILADELPHIA (February 2, 2003) -- 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 isnt new, but weve 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.
Murphy and her colleagues have known about the two p53 variants, but how the differences affect p53s ability to suppress tumor development was not previously understood until now.
People have one form or another of p53, says Murphy. The p53 variant containing the amino acid called arginine is better at killing out-of-control cells. The other p53 variant with the amino acid proline is less capable of stopping errant cells. When we asked if the two forms might function differently, the answer was a resounding yes.
In terms of treating cancer, patients could potentially be typed for the kind of p53 they have, some day allowing physicians to tailor their therapy.Page: 1 2 3 Related biology news :1
Contact: Karen Mallet
Fox Chase Cancer Center
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