Background: Inflammatory bowel disease (IBD; including ulcerative colitis and Crohn's disease) is associated with an increased risk for colorectal cancer (CRC). Chronic mucosal inflammation is a key factor in the onset of carcinogenesis in IBD patients. Although most gene alterations that cause sporadic CRCs also occur in patients with IBD-associated CRC, some gene sequences and mutation frequencies differ between sporadic CRCs and IBD-associated CRCs.
Summary: This review explores the incidence of CRC in IBD patients, with the goal of identifying the risk and protective factors for CRC in order to facilitate dysplasia management via individualized surveillance strategies.
Key message: The incidence of CRC is higher among IBD patients. Identifying the risk and protective factors for CRC will facilitate dysplasia management via individualized surveillance strategies.
Practical implications: Several risk factors, including active inflammation, the coexistence of primary sclerosing cholangitis, a family history of sporadic CRC and the extent and duration of colonic disease, can lead to the development of CRC in patients with IBD. These risk factors should be utilized in individualized surveillance strategies to lower CRC incidence among IBD patients. Use of 5-aminosalicylic acid may play an important role in CRC prevention. Until newer, more reliable markers of IBD-associated CRC risk are found, dysplasia will continue to be the best marker of CRC risk in IBD. Dysplasia management continues to play a key role in preventing the progression of carcinogenesis.
Keywords: Colorectal cancer; Crohn's disease; Dysplasia-associated lesion or mass; Surveillance; Ulcerative colitis.