From Inflammation to Cancer in Inflammatory Bowel Disease: Molecular Perspectives

Inflammatory bowel diseases (IBD) are associated with an increased risk of colitis-associated colorectal carcinoma (CAC). CAC is one of the most important causes of morbidity and mortality in patients with Crohn's disease and ulcerative colitis. The aim of the present review was to discuss the most important signaling pathways and genetic alterations involved in carcinogenesis related to IBD, focusing on the molecular aspects of cancer stem cell physiology and the impact of the inflammatory microenvironment. Molecular mechanisms involved in CAC development differ from those in sporadic colorectal cancer, reflecting the prominent role of inflammation-induced carcinogenesis in the development of CAC. The alteration of the physiological microenvironment is thought to be responsible for the initiation of carcinogenesis in IBD. Furthermore, cancer stem cells seem to have a fundamental role in the generation and growth of CAC. We also address prevention and treatment modalities of CAC and its involvement in IBD.