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Jefferson scientists find guardian gene's choices crucial to stopping cancer process

player in the cancerous process it's nearly always mutated or inactivated in cancer that continuing to understand more about how it works will likely have significant implications for cancer research," says Dr. McMahon. "We wouldlike to understand the interplay between this newly identified pathway and others involved in p53 and cancer.

"Since p53 can make this decision, this might give some insight into which function of p53 is more important in which tissues," says co-author Stephen Sykes, a Ph.D. candidate at the University of Pennsylvania. "For example, K120 (lysine 120) mutations cause tumors in the prostate, but are not so much involved in causing immune system cancers such as lymphomas. That could suggest that p53's potential to cause cell death could be more important in certain tissues than in others. In the future, if someone could develop therapies that could specifically activate p53's potential to drive programmed cell death versus the cell cycle arrest potential, it might influence how a doctor might choose to treat a certain type of cancer.

"This may potentially enable the development of a cancer drug that would stimulate the enzymes to promote this modification driving p53 to apoptosis."


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Contact: Steve Benowitz
steven.benowitz@jefferson.edu
215-955-5291
Thomas Jefferson University
5-Jan-2007


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