New York, N.Y., September 1, 1998 -- In a study of the protein p27, researchers at Memorial Sloan-Kettering Cancer Center have confirmed the existence of at least two different types of prostate cancer. One is a more aggressive form of the disease with a higher rate of recurrence and poorer long term survival. Researchers believe that this information can help in determining the patient's prognosis which may affect treatment selection.
Researchers also discovered that p27 plays a distinct role in Benign Prostate Hyperplasia (BPH) which was found to be genetically different from prostate cancer. This supports the thesis that it is not a precursor to the development of prostate cancer.
The study, published in the September Journal of the National Cancer Institute, involved the examination of the levels of p27 protein in one hundred and thirty tissue samples of patients with prostate cancer as well as samples from normal men and patients with BPH.
The p27 protein, first discovered by study co-authors Dr. Joan Massagu, chairman of the Cell Biology Program at Memorial Sloan-Kettering and Dr. Andrew Koff of the Molecular Biology Program, is one of the proteins generically called a cell cycle inhibitor. It is a potential tumor suppressor. Normal prostate tissue has abundant amounts of both p27 protein and its messenger RNA (p27KIP1 mRNA), the intermediary between the gene and the protein. However, both messenger and protein are undetectable in patients with BPH. In contrast, patients with prostate cancer have abundant p27KIP1mRNA but p27 protein levels were variable - high in some cases or very low to undetectable in others. Investigators found that prostate cancers with the lower levels of p27 were more aggressive.
"Our study reinforces previous research that suggests that prostate cancer can
develop along two different pathways, one involving the loss of p27 and the
other using processes that circumvent the growth-suppressive effects of p27,"
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Contact: Joanne Nicholas
nicholaj@mskcc.org
(212) 639-3573
Memorial Sloan-Kettering Cancer Center
1-Sep-1998