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Colorectal cancer (CRC) is one of the most common causes of cancer-related deaths worldwide. As with other cancers, CRC is a genetic disease, however, several risk factors including diet and chronic colitis predispose to the disease. Mutations in the tumor suppressor adenomatous polyposis coli (APC) initiate most cases of CRC. Recent data from mouse models suggest that APC mutations and colitis are not completely independent factors in colorectal carcinogenesis. Here, we review the evidence supporting an interaction between APC muta- tions and chronic colitis. We will also discuss possible pathophysiologic mechanisms behind this interaction.

New insights from animal models of colon cancer: inflammation control as a new facet on the tumor suppressor APC gem