Abstract
Chronic inflammation plays a pivotal role in the development of colorectal cancer (CRC) in patients with inflammatory bowel disease (IBD). An orchestrated interplay of immune cells with numerous inflammatory mediators including reactive oxygen and nitrogen species, cyclooxygenase 2, and several cytokines promotes colitis-associated cancer (CAC). Recent findings have shown that inflammatory pathways not only are important in the development of CAC but are also involved in the pathogenesis of sporadic CRC. Hereby, we review the existing experimental and clinical evidence that suggest a link between inflammation and tumorigenesis in sporadic CRC.