Scientists have discovered that induction of a gene known as MDA-7/IL-24 is the molecular mechanism that enables nonsteroidal anti-inflammatory drugs (NSAIDs) to halt the// growth of cancer cells, a finding that could eventually lead to the development of targeted cancer treatments. Led by researchers at Beth Israel Deaconess Medical Center (BIDMC), in collaboration with scientists at Columbia University Medical Center, the new findings provide the answer to the long-puzzling question: How does this popular class of pain killers protect people from developing this deadly disease? The study appears in the Dec. 15 issue of the journal Cancer Research.

“Although observational studies had previously demonstrated that NSAIDs [such as aspirin, ibuprofen and sulindac] might be effective in the prevention and treatment of several common cancers, it wasn’t at all clear how this was happening,” explains the study’s senior author Towia Libermann, PhD, Director of the BIDMC Genomics Center and Associate Professor of Medicine at Harvard Medical School (HMS). “Now, after treating a number of different types of cancer cells in culture with a whole set of NSAIDs, we can point to this single gene which, when upregulated, kills cancer cells while sparing normal, healthy cells.” In recent years, a great deal of attention has focused on the link between inflammation and cancer. As the body’s immune response to tissue damage, acute inflammation serves as a natural defense to guard against injury or infection. However, in cases of chronic inflammation – for example, inflammatory bowel disease – certain signaling pathways that modulate the inflammatory processes become “stuck” in an activated state. Among other outcomes, this course of events leads to the release of molecules that enhance carcinogenesis and tumor progression at the site of the damage.

According to Libermann, it was these observations that originally prompted clinical and epidemiological researchers
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