(RxWiki News) Prostate tumors can often be controlled by hormone-blocking drugs, but they may become resistant after a few years. A molecular switch could offer a new means for cancer control.
EZH2 is a protein that increases in prostate cancer that no longer responds to hormone-based therapy.
Scientists have recently identified a molecular mechanism in this protein that enables advanced tumors to spread. This discovery opens the pathway to potential new treatment.
"Stay informed about new cancer treatments."
Myles Brown, MD, professor of medicine at Harvard Medical School and director of the Center for Functional Cancer Epigenetics at the Dana-Farber Cancer Institute in Boston, led the research.
The lab study revealed that the EZH2 protein is activating cell-growth genes in advanced prostate cancer, even in the absence of male hormones called androgens.
EZH2 protein levels dramatically increase in late-stage castration-resistant prostate cancer (CRPC). Spurred by hormone production, this type of cancer can often be suppressed for a time through “surgical castration” or by administering hormone-blocking drugs.
Some hormone-based therapy drugs are leuprolide (Lupron, Viadur, Eligard), goserelin (Zoladex), triptorelin (Trelstar) and histrelin (Vantas).
After a few years, these cancers often change and no longer respond to hormone-based therapy. Investigators found that EZH2 may be the culprit for this cancer growth. The protein appears to turn on a function that spurs the spread of these tumors.
Based on these results, the authors of the study suggest that drugs designed to inhibit this function of EZH2 might be effective for treating CRPC tumors.
EZH2 is part of a protein complex that normally shuts off the expression of genes. Dr. Brown and his colleagues found that the protein is working in a different mode in prostate cancer, activating cell growth.
Drugs aimed at stopping EZH2 activity are being tested in other cancers, where they are designed to block the protein’s gene-suppressing role.
Dr. Brown added that the EZH2 protein itself is turned on by a molecular signaling pathway known as PI3K, or PI3 kinase. Several PI3K inhibiting drugs are in clinical trials at present. Brown said that a combination of drugs to inhibit both that pathway and the EZH2 protein might be another way to attack these resistant prostate cancers.
This study was published in December in Science.
