The discovery of a pathway through which non-inflammatory drugs can inhibit development of colon cancer may move researchers one step closer to more effective prevention or treatment of the disease, according to an article in the Proceedings for the 2003 Annual Meeting of the American Association for Cancer Research.

The American team found that colorectal cancer cells have elevated levels of the immune system protein called IL-6; they determined that the protein triggers carcinogenesis by activating another protein (called STAT1), which prevents normal cell death in the lining of the colon.

David Frank, MD, PhD, and his American colleagues found that several nonsteroidal anti-inflammatory drugs (namely, ibuprofen, aspirin, and sulindac) block the activation of STAT1 by IL-6 in colon cancer cells. Applications of butyrate, which is produced when dietary fiber is metabolized, also blocks IL-6 activity, although through a different signaling pathway.

The research team is currently looking for ways to block activity of the STAT1 protein that might have clinical benefit for patients with colorectal cancer.