βarrestin2, a protein used for the purpose of regulation of androgen receptors’ expression, can be a new focal point for staging and curing testosterone-fueled prostate cancer, as per medical College of Georgia researchers. The study findings were reported in Proceedings of the National Academy of Sciences Online Early Edition.

As per study’s corresponding author, Dr. Yehia Daaka, Distinguished Chair in Oncologic Pathology in the MCG School of Medicine, an increase in the number of androgen receptors was what considered to be behind the growth of prostate cancer progression in men with advanced disease.

From Sciencedaily.com:

With increased numbers of androgen receptors, prostate cancer can make use of the limited testosterone available after a diseased prostate gland is removed or after testosterone production is blocked by drug therapy. In fact, the increased number of androgen receptors may mutate so they can start feeding off other steroids or even growth factors, Dr. Daaka says.

These wily skills help explain why cancer returns despite initially promising treatment results.

“It is clear that signaling by the androgen receptor is paramount for not only the initiation but also the progression of the disease, including escape to a hormone-refractory disease,” he says. Moves androgen receptors make to support cancer growth make it “unbeatable at this point,” for some patients.

However increased levels of βarrestin2 appear to halt the potentially deadly increase in androgen receptor expression, the MCG research team has found.

Dr. Daaka, a Georgia Cancer Coalition Distinguished Cancer Scholar, remarked that initiation and progression of prostate cancer can be regulated by regulated by expression or non-expression of activation or repression of the androgen receptors’ co-factors.

The involved collaborators included Dr. Vijayabaskar Lakshmikanthan, postdoctoral fellow; Dr. Lin Zou, former postdoctoral fellow;  Jae Kim, graduate student; Dr. Nidia C. Messias, assistant professor; and Dr. Zhongzhen Nie, assistant professor; from the MCG Department of Pathology; and Drs. Allison Michal and Jeffrey L. Benovic from Thomas Jefferson University.

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