Prevalence of polyp formation on follow-up, albeit high in this study, did not significantly differ across subgroups this website (62.5%, 50%, and 49%, respectively) indicating IBD-associated

dysplasia may be effectively treated endoscopically. Indeed, over the past few years, endoscopic mucosal resection and endoscopic submucosal dissection resection techniques proved to be increasingly safe and effective in the Western practice.36, 37 and 38 A study examining the effectiveness of endoscopic resection of NP-CRNs found that 93% of those larger than 10 mm were successfully resected.36 Residual neoplasia was identified in 10% of cases on the first follow-up examination, although complete resection was obtained in all cases after one to three follow-up examinations. Likewise, Buchner and colleagues37 found that large sessile and NP-CRNs could be managed endoscopically in 91% of cases, with a perforation rate of 0.4% and a bleeding rate of 11%. Because 9%23 to 50%38 of the sporadic interval CRCs are thought to be caused by an ineffective polyp resection, the GPCR & G Protein inhibitor precise contribution of this factor to the genesis of interval CRCs in patients with IBD needs further elucidation. Adherence to colonoscopic surveillance guidelines is

indeed vital, but seems to be often problematic.39, 40, 41 and 42 There are several caveats to keep in mind, foremost of which is the patient’s understanding of the cancer risk.43 and 44 Disease flares and presence of comorbidity may further reduce the compliance to surveillance. Because the presence of disease activity challenges the endoscopic and histologic

appreciation of dysplasia, colonoscopic surveillance should be ideally performed in the quiescent phase. However, surveillance should not be delayed too long, because those with more active disease carry a greater risk of developing CRC. With regard to bowel preparation, a low-residue diet the days before the procedure in conjunction with split-dose polyethylene glycol solutions is often sufficient for adequate cleansing, without inducing inflammation. The precise biologic events underlying chronic inflammation Decitabine chemical structure and leading to a faster progression to CRC are presently unknown and need further exploration. A subset of dysplastic lesions identified in patients with IBD harbor a villous phenotype, as illustrated in Fig. 2. Such macroscopic features have been suggested to represent a red flag for the presence of invasive CRC, especially of colloid subtype.45 Other CRCs harbor signet ring cells, features associated with a more aggressive biologic behavior. Fig. 3 illustrates a small signet ring cell carcinoma that displayed clear signs of local invasion.