University of Pennsylvania Cancer Center
Last Modified: May 16, 1999
The function of the p53 gene, which induces damaged cells to activate "programmed cell death," is lost as cancer progresses and spreads. Therefore, replacing p53 to increase production of its normal protein, which would lead to cancer cell death, could reduce the size of prostate tumors, said Logothetis, who added that this strategy has been shown to be feasible in other cancer types, such as lung and head and neck cancer.
The gene was delivered by injection into the prostate, and the patients had a prostatectomy (removal of the prostate gland) performed following therapy. The investigators were able to demonstrate on serial examination before the prostatectomy that seven of the 26 treated cancers reduced in size. A total of 30 patients are being treated but some have not completed the therapy schedule. Logothetis and his research colleagues view the results of the study as encouraging evidence in support of the original hypothesis, and says it will serve as the foundation for combination therapy incorporating p53 gene therapy in the treatment of prostate cancer.
Aug 31, 2010 - Researchers have discovered a mechanism by which adenoviruses breach cellular defenses, and this could help explain how p53 tumor-suppressor genes are disabled in cancer cells and point the way to the development of new, more effective targeted cancer therapies; these findings have been published in the Aug. 26 issue of Nature.
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