As molecular pathways of colon carcinogenesis continue to be defined for high risk hereditary colon cancer syndromes and for average risk sporadic colon cancers, it seems that colon carcinogenesis in the setting of chronic idiopathic inflammatory bowel disease (IBD) may be unique.1 Although to some extent this notion seems intuitive because of the substrate of chronic inflammation from which these cancers arise, it is nevertheless curious that despite the setting of chronic inflammation, colon cancers occurring in patients with colitis share several features in common with those that arise in patients with hereditary non-polyposis colorectal cancer (HNPCC). For example, in both conditions there is a tendency for the colorectal cancers to affect young individuals, be multifocal, show a proximal colonic distribution, and display mucinous, signet-ring cell or undifferentiated histology. In addition, HNPCC colorectal cancers often have a rim of surrounding inflammation, referred to as a Crohn's-like reaction. These clinicopathological similarities have prompted some investigators to explore whether colitis associated cancers might in fact share a common molecular pathogenesis with HNPCC colorectal cancers.

Colorectal cancers in patients with HNPCC occur by virtue of a defective ability to repair DNA base pair mismatches. This results in DNA replication errors that have the net effect of altering genes that are critical for maintaining normal growth and behaviour of colonic …