Prostate Cancer Switch May Yield Map Of Cancer Machinery, Targets For Drugs

DURHAM, N.C. -- A team of molecular biologists has pinpointed a genetic switch in prostate cancer cells that may play a role in triggering a quiescent tumor to erupt into an invasive, deadly cancer that spreads throughout the body.

The scientists said discovery of this single genetic switch could open a research pathway that might well lead to a road map of the complex changes prostate cancer cells undergo in their progression to a deadly form. Such a road map would yield not only molecular markers that would allow physicians to better pinpoint the stage of a prostate cancer, but also new drugs to kill cancer cells at earlier stages, the researchers said.

Prostate cancers are distinguished by their tendency to linger at a relatively benign stage for many years, but to suddenly transform into a deadly form that spreads, or metastasises, throughout the body.

The scientists are Russ Carstens and Mariano Garcia-Blanco of the Duke University Medical Center department of pharmacology and cancer biology, and Wallace McKeehan of Texas A&M University. They published their findings in the April issue of Molecular and Cellular Biology. Their work is supported by the National Institutes of Health, the Duke Comprehensive Cancer Center, the American Heart Association and the Keck Foundation, which supports the Levine Science Research Center, where the work was performed.

Working with rat prostate cancer cells, the scientists discovered the molecular basis for a genetic switch that governs whether a cancer cell generates one or another form of a protein receptor molecule called FGF-R2 (Fibroblast Growth Factor Receptor 2) that festoons the surface of the cell.

These receptors are molecular locks, into which fits a protein called a growth factor, secreted by another cell in the prostate. As long as the FGF-R2 receptor is of one type -- called IIIb -- the cancer cell is relatively

Contact: Dennis Meredith
Duke University

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