The two major clinically defined forms of inflammatory bowel disease (IBD), Crohn's disease (CD) and ulcerative colitis (UC), are associated with an increased risk for colon cancer. The increased risk of developing CRC is one of the most serious long-term complications faced by patients with UC and Crohn's colitis. UC, in particular, carries a high risk for malignant transformation, with UC patients being up to 30 times more likely to develop colorectal cancer (CRC) and three times more likely to die from CRC compared with the general population (Gillen et al., 1994; Greenstein, 2000; Rhodes and Campbell, 2002a). Risk factors for IBD associated CRC in UC patients include: disease duration greater than 8 years, pancolitis, biopsy-proven colonic dysplasia, and the presence of primary sclerosing cholangitis affecting the liver (Bernstein et al., 2001; Broome et al., 1995; Gillen et al., 1994). There is also an increased risk of IBD-associated colon carcinoma for patients with CD (Greenstein et al., 1981; Weedon et al., 1973; Gyde et al., 1980; Bernstein et al., 2001). Feagin et al. (Feagins et al., 2009) reported that individuals with Crohn's colitis are believed to have a 4.5-fold higher relative risk of developing CRC than the general population. Little is known about the underlying genetic changes that occur as IBD progresses from benign mucosa to dysplasia and eventually to invasive CRC. A partial explanation for this progression may be a genetic basis for the increased risk of CRC in IBD patients (Kraus and Arber, 2009). It is possible that the high levels of inflammatory substrates produced may contribute to the development and progression of CRC (Kraus and Arber, 2009). In addition, the pathogenesis of IBD-associated CRC has been poorly described as compared to sporadic CRC. Interestingly, different mechanisms are suggested for each (i.e., TP53; MIM# 191170) mutations occurring late in sporadic CRC, while appearing early in the course of IBD-associated CRC (Riddell et al., 1983).
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