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URMC / Pathology & Laboratory Medicine / Read Our Blog / April 2016 / Is It Time for New Strategies to Treat Aggressive Prostate Cancer?

Is It Time for New Strategies to Treat Aggressive Prostate Cancer?

A new URMC study confirms that androgen deprivation therapy, which initially shrinks aggressive prostate tumors, is a double-edged sword that ultimately might fuel the spread of cancer.

It’s a controversial topic that has been investigated for years by Chawnshang Chang, Ph.D., the scientist holds yellow vial in labGeorge Hoyt Whipple Distinguished Professor of Pathology, Urology, and Radiation Oncology at the University of Rochester and Wilmot Cancer Institute. As his research gained momentum, other investigators across the country began reporting similar results about androgen deprivation therapy (ADT).  In fact, a recent review in the journal Cancer Letters (where Chang’s research was also published), calls for a fundamental shift in the way advanced prostate cancer is treated.

“It’s the right time in history for this, and I’m very happy that other major research groups are confirming our initial observations that ADT actually promotes metastasis,” Chang said.

Early stage prostate cancer is usually treated successfully with surgery and/or radiation therapy. Some early cases don’t even require treatment beyond careful monitoring. In advanced disease, however, ADT remains the standard of care.

Chang’s latest study in Cancer Letters suggests a new mechanism through which ADT inadvertently spreads cancer—by boosting the stem cell population associated with prostate tumors. Previous studies have suggested that a larger stem cell population usually feeds a more aggressive cancer, Chang said, although his study does not specifically address that issue.

Chang is also developing an alternative therapy to ADT known as ASC-J9, which is a chemically modified derivative of the spice ginger. The recent data suggest that in preclinical testing, ASC-J9 suppresses aggressive prostate tumors and their stem cell populations by altering an important protein pathway known as EZH2/STAT3.

Bethany Bushen | 4/27/2016

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