Replacing P53 Gene in Prostate Cancer Helps Shrink Tumors
May 16, 1999 Dr. Christopher Logothetis and his team of investigators at M.D. Anderson Cancer Center in Texas have demonstrated evidence that replacing the p53 gene may shrink prostate cancers.
     Normally, the p53 gene performs the task of triggering damaged cells go into apoptosis, or "programmed cell death." But as cancer progresses and spreads, the gene loses the power to do this.
     Logothetis was testing to find out if replacing p53 in a prostate cancer patient would increase production of its normal protein, and restore the process of cancer cell death. This could reduce the size of prostate tumors, Logothetis said. This strategy, Logthetis said, 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.
     Thirty patients in all 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. He says these findings will serve as the foundation for combination therapy incorporating p53 gene therapy in the treatment of prostate cancer.