Ulcerative colitis and colon cancer: biology and surveillance

Abstract

The risk of colorectal carcinoma is increased among patients with longstanding ulcerative colitis and Crohn's disease. The development of cancer in inflammatory bowel disease is hypothesized to evolve by a multistep process involving genetic instability, clonal expansion and the development of a malignant phenotype. The contribution of nutritional factors such as folate deficiency is of great interest; molecular genetic mechanisms are under study. In contrast to sporadic colorectal carcinoma, carcinomas in ulcerative colitis are associated with a long prior history of chronic inflammation and the subsequent development of epithelial dysplasia. Dysplasia is defined as an unequivocal neoplastic alteration of the colonic mucosa. The object of surveillance is prevention of death from cancer by detection at a premalignant or early curable stage. Patients at greatest risk of cancer who customarily undergo endoscopic surveillance are those with extensive colitis of more than 8 years duration. Dysplastic epithelium may occur in flat mucosa, and may produce a plaque or a nodular/villiform appearance. Dysplasia is not present in all patients with cancer in colitis. It is important to develop more sensitive and specific markers for the presence of precancer or cancer in colitis. Under study are proliferation-associated markers detected by immunohistochemistry, lectin binding, flow cytometry and laser-induced fluorescence coupled with endoscopy.