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Study Explains How NSAIDs Halt Cancer Growth

odel of prostate cancer to demonstrate that when MDA-7/IL-24 was blocked, the anti-cancer effects of the NSAIDs were diminished.

Finally, building on their earlier work demonstrating the relevance of GADD45 (Growth Arrest DNA Damage) family members to cancer cell death (as well as previous work by study coauthor Paul Fisher, MPh, PhD, of Columbia University Medical Center) Libermann and Zerbini identified GADD45 alpha and gamma as the critical mediators of this course of events, showing that the ability of NSAIDs to induce apoptosis was dependent on their abilities to induce MDA-7/IL-24 expression, leading to enhanced GADD45 alpha and gamma expression.

“Current clinical trials are evaluating a range of NSAIDs for a variety of cancers without any clear vision of the best way to use them,” notes Libermann. “The fact that upregulation of this single gene – MDA-7/IL-24 -- correlated not only with cell death induction of numerous types of cancer but also among various diverse classes of NSAIDs, makes this discovery particularly exciting. The level of MDA-7/IL-24 gene expression in cancer patients may emerge as a new biomarker for monitoring patients’ responses to certain therapies, and may help determine whether drugs such as NSAIDs are hitting their intended targets.”

In addition to Libermann, Zerbini and Fisher, study coauthors include BIDMC investigators Akos Czibere, MD, Yihong Wang, MD, Hasan Otu, PhD, Marie Joseph, Yuko Takayasu, MD, Moriah Silver, Xuesong Gu, PhD, Kriangsak Ruchusatsawat, PhD, Linglin Li, MSc, and Jin-Rong Zhou, PhD; Ricardo Correa, PhD, of The Salk Institute for Biological Studies in La Jolla, California; and Devanand Sarkar, PhD, of the Columbia University Medical Center, College of Physicians and Surgeons, New York. This study was funded, in part, by grants from the National Institutes of Health, the U.S. Department of Defense, the Hershey Foundation, the Samuel Waxman Cancer Research Foundation and the Chernow En
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