Building on earlier studies that have shown that common painkillers known as NSAIDs (non-steroidal anti-inflammatory drugs) can reduce the risk of colon cancer in healthy people, researchers at Dana-Farber Cancer Institute have identified a mechanism by which NSAIDs inhibit the development of colon cancer. Compared with normal cells, colorectal cancer cells have abnormally high levels of an immune system protein, IL-6. David Frank, MD, PhD, and his Dana-Farber colleagues have discovered that IL-6 triggers malignant growth by activating a protein called STAT1, which transmits signals that prevent the normal scheduled death of cells in the colon.From the Dana-Farber Cancer Institute:Study sheds new light on how common painkillers prevent colon cancer
Findings could lead to new treatments for the disease
Building on earlier studies that have shown that common painkillers known as NSAIDs (non-steroidal anti-inflammatory drugs) can reduce the risk of colon cancer in healthy people, researchers at Dana-Farber Cancer Institute have identified a mechanism by which NSAIDs inhibit the development of colon cancer.
Compared with normal cells, colorectal cancer cells have abnormally high levels of an immune system protein, IL-6. David Frank, MD, PhD, and his Dana-Farber colleagues have discovered that IL-6 triggers malignant growth by activating a protein called STAT1, which transmits signals that prevent the normal scheduled death of cells in the colon.
The findings are published in the Proceedings for the 2003 Annual Meeting of the American Association for Cancer Research.
Frank and his colleagues found that NSAIDs block the IL-6 activation of STAT1, throwing a wrench into the signaling pathway leading to cancer. They showed this by treating colon cancer cells in the laboratory with NSAIDs such as ibuprofen, aspirin and sulindac. They also applied butyrate, a chemical that’s produced when the body metabolizes dietary fiber, which also helps protect against colon cancer. Butyrate also blocked IL-6 activity, but through a different signaling pathway.
With these findings in hand, Frank, who is an assistant professor of medicine at Harvard Medical School, said that he and his colleagues are studying ways to block the STAT1 protein in patients who have already developed colorectal cancers.
Dana-Farber Cancer Institute is a principal teaching affiliate of the Harvard Medical School and is among the leading cancer research and care centers in the United States. It is a founding member of the Dana-Farber/Harvard Cancer Center (DF/HCC), designated a comprehensive cancer center by the National Cancer Institute.
