Abstract
It is recognized that ulcerative colitis (UC) predisposes to the development of colorectal adenocarcinoma (CRC), and the molecular pathway for this process differs from that for sporadic CRCs. However, several important details regarding the risk factors for and the molecular changes underlying UC-related colorectal carcinogenesis have only come to light lately. First, recent data suggest environmental factors related to long-standing inflammation contribute more to this increased cancer risk than an inherited susceptibility. Second, molecular changes that may represent the first steps in the development of neoplasia are being increasingly identified in non-dysplastic, colitic mucosa. Third, there is now good evidence suggesting that UC-related CRC may develop along more than one molecular pathway. These emerging data will hopefully contribute to attempts to prevent the development of UC-related CRC, e.g. through refining surveillance programmes. Details of the molecular heterogeneity of UC-related dysplasia and CRC may also help develop reliable tools for diagnosing the former and for predicting the behaviour of the latter. Finally, there is increasing awareness of non-epithelial colorectal malignancies which are associated with UC and may potentially increase in incidence with changes in the medical management of this inflammatory disease.
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