Gene Affects Response of Prostate Tumors to Radiation

The study was published in the July 2002 issue of the International Journal of Radiation Oncology, Biology, and Physics.

Researchers from the University of Wisconsin Comprehensive Cancer Center (Madison, USA) sought to learn the cause of treatment failures following radiation therapy in some prostate cancer patients. They focused on the p53 gene, hypothesizing that its active or inactive state might play a role in the response of patients. They established normal or abnormal p53 status in a group of 53 favorable-to-intermediate risk prostate cancer patients previously treated with radiation. The patients were selected for relatively low pretreatment prostate-specific-antigen (PSA) and Gleason scores to reduce the likelihood of nonlocalized disease.

The status of p53 was immunohistochemically assessed in paraffin-embedded pretreatment biopsy specimens. With this type of measurement, a high p53 labeling index indicates abnormal status. The total group of 53 patients showed a biochemical failure rate after radiotherapy of 35% at five years. Of these, 38% had a greater-than-10% labeling index for p53, and patients with these higher labeling indices demonstrated significantly higher PSA failure rates.

"Identifying abnormal p53 status through biopsy before treatment begins may allow the treatment team to better assess whether conventional radiation therapy will be adequate or whether other options, such as more aggressive radiation dose escalation, surgery, or perhaps even p53 targeted therapy, should be considered,” said Mark a Ritter, M.D., Ph.D., of the department of human oncology at the center, and lead author.




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