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How some prostate tumors resist treatment -- and how it might be fixed
Date:3/18/2013

ation. That removes the brake, allowing the recycling of inactive androgen receptor to active status. As a result, prostate cancer cells produce more active androgen receptors, which render them resistant to hormone therapy.

Clinical relevance

Ronai and colleagues wondered if Siah2 plays the same role in real-life castration-resistant prostate cancer as they had observed in the lab. Using samples provided by collaborators at the Vancouver Prostate Centre at the University of British Columbia, the team determined that human castration-resistant prostate tumors have abnormally high levels of Siah2 and select androgen receptor targets. This finding underscores the clinical significance of the castration-resistance mechanism they uncovered.

Ronai and his team also looked at what happens when they inhibit Siah2. To do this, they used three different animal models. In each case, inhibiting Siah2 restored prostate tumors' sensitivity to hormone therapy. With Siah2 out of the picture, prostate tumors regressed during hormone therapy.

"We see Siah2 not only as a biomarkera way to track the development and progression of castration-resistancebut also as a potential therapeutic target for prostate cancer," explained Jianfei Qi, Ph.D., staff scientist in Ronai's lab and first author of the paper.


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Contact: Heather Buschman
hbuschman@sanfordburnham.org
858-795-5343
Sanford-Burnham Medical Research Institute
Source:Eurekalert  

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