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Tracy Hampton, PhD

JAMA. 2007;297:459.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

Researchers at Beth Israel Deaconess Medical Center, in Boston, in collaboration with scientists at the Salk Institute for Biological Studies, in La Jolla, Calif, and Columbia University Medical Center, in New York City, have discovered a mechanism by which nonsteroidal anti-inflammatory drugs (NSAIDs) halt cancer growth, a finding that could lead to new tests for monitoring patients' responses to these therapies and to safer drugs that act in a similar manner (Zerbini LF et al. Cancer Res. 2006;66:11922-11931).

While NSAIDs are known to exhibit anticancer effects through inducing cell death by inhibition of cyclooxygenase enzymes, scientists have suspected that other antitumor mechanisms are at play.

Using gene expression analyses, the researchers found that exposure to NSAIDs caused cancer cells to increase expression of the gene that encodes a cancer-specific cytokine, MDA-7/IL-24 (melanoma differentiation associated gene 7/interleukin 24). This cytokine induces cell death and inhibits tumor growth, . . . [Full Text of this Article]