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Editor's Corner
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volume 7 | issue 4
April 2008Subscribe to this journal for $129/year
Prostate cancer is the leading cause of cancer related deaths in men. The American Cancer Society estimates that there will be 186,320 new cases in 2008 with over 28,000 deaths. Although starving prostate cancer cells of androgen can inhibit tumor growth, clones of androgen-independent cancer cells eventually arise. Recent studies have elucidated some of the mechanisms by which prostate cancer cells progress to androgen-independent survival. In this month's issue of Cancer Biology & Therapy, Hamed and colleagues expand upon the observation that hCG radiosensitizes prostate cancer cells by upregulating the ERBB1-MEK1-ERK1/2 pathway. They examine the ability of hCG and lovastatin, an HMG CoA reductase inhibitor, to radiosensitize prostate cancer cells. This month's cover shows tumor sections stained for activated caspase-3 (an apoptotic marker) from mice treated with a combination of hCG and lovastatin. These tumors show enhanced apoptosis and dramatically decreased proliferation compared to single modality treatment. To learn more about the survival of prostate tumors when radiation was added to the hCG and lovastatin regimen see the manuscript by Hamed and colleagues and the commentary by Franklin and McCubrey.




