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Vitamin D, NSAIDS provide double whammy against prostate cancer, Stanford study finds

only lung cancer kills more men. Although prostate cancer is often a slow-growing, noninvasive type of cancer, there are some cases where a deadly migration of cancer cells invades other parts of the body. The standard treatment for such cases is hormone therapy, but that treatment ultimately does not work for most patients. Slowing the growth of the prostate cancer cells could buy time for patients before beginning this last-ditch therapy.

Over the course of Feldman's years of vitamin D research, he and others had determined that the vitamin has several actions that make it useful in cancer therapy. While a great deal is now known about these effects, there is still much to be learned about how the vitamin stymies tumor growth.

To get an idea of what calcitriol does on a genetic level to halt tumor growth, the researchers used a cDNA microarray, a tool that provides an overview of the genetic changes that occur when prostate cancer cells react to calcitriol. The researchers discovered that two of the affected genes are critical in the production and breakdown of prostaglandins - hormones that cause a range of physiological effects, including inflammation. Inflammation, in turn, is also associated with cancer growth.

Like calcitriol, NSAIDs also block prostaglandin production. Thus, it seemed logical to test calcitriol in various combinations with NSAIDs to see if the double whammy could knock out prostate cancer better than either drug alone, explained study leader Jacqueline Moreno, PhD, a postdoctoral scholar in Feldman's lab.

When the researchers began the study, which was done on cells in culture, they were using selective NSAIDs, such as Vioxx and Celebrex. These drugs specifically target the prostaglandin pathway, reducing the gastrointestinal side effects of the nonselective NSAIDs. But after Vioxx was pulled from the market last year due to cardiovascular risks, the researchers switched to using two nonselective N
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Contact: Mitzi Baker
mabaker@stanford.edu
650-725-2106
Stanford University Medical Center
1-Sep-2005


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