Colorectal cancer in inflammatory bowel disease: molecular and clinical considerations

Abstract

Adenocarcinoma of the colon is an accepted and feared complication of chronic ulcerative colitis (UC) and colonic Crohn's disease (CD). When cancer is identified, surgery is necessary, and unlike with sporadic colorectal cancer (CRC), in which partial colectomy is effective, proctocolectomy is required. As CRC is a rare complication of these diseases, studies of the pathogenesis are limited primarily to observational studies; thus, the mechanism and molecular events that lead to neoplastic change are not fully understood or well known. Precancerous dysplasia has been associated with concurrent or future CRC in UC and, although less studied, in CD, and is therefore considered a marker of cancer risk in inflammatory bowel disease (IBD). Risk factors for dysplasia and CRC in IBD include longer duration of disease, greater extent of disease, younger age at diagnosis, diagnosis with primary sclerosing cholangitis (PSC), family history of CRC, and possibly backwash ileitis and degree of inflammation of the bowel over time. Prevention of cancer in IBD has been focused on secondary measures of identifying dysplasia in flat mucosa or protruding lesions during surveillance colonoscopy with random biopsies and, when confirmed, performing proctocolectomy. Studies of primary prevention of dysplasia and CRC using chemopreventive agents have suggested a possible benefit with a number of agents. These include ursodeoxycholic acid (in patients with PSC and UC), aminosalicylates, and possibly statins.