Replacing P53 Gene in Prostate Cancer Helps Shrink Tumors

University of Pennsylvania Cancer Center
Ultima Vez Modificado: 16 de mayo del 1999

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A team of investigators from the M.D. Anderson Cancer Center, led by Dr. Christopher Logothetis, has demonstrated evidence that replacement of the p53 gene may shrink prostate cancers.

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.


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