Senescence Signaling Through p53

Ronald Gary, Ph.D. (University of Nevada, Las Vegas)

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Cancer comes in many forms, and it can occur in virtually any type of tissue (lung, brain, breast, prostate, blood, etc.). At the molecular level, even cancers of the same tissue type vary greatly from one patient to the next. But one defining feature that is common to all types of cancers is that these cells divide and multiply inappropriately, ignoring the usual constraints that prevent excessive growth. Most cancer chemotherapies attempt to kill the cancer cells outright, but if it were possible to simply stop the tumor cells from multiplying, such an approach might be equally effective. Drugs that block cell division without actually killing the cells might be preferable to current chemo agents, because the new approach would probably produce milder side effects and be better tolerated by patients. We are studying pharmacological agents that cause cells to become senescent. In this state, the cells remain alive, but they produce high levels of p21, p16, and SA- ß-gal, and they are unable to reproduce through cell division.