A 28-year-old male with history of ulcerative pancolitis and primary sclerosing cholangitis diagnosed in 1997 who had no dysplasia on surveillance colonoscopy 2 years prior to this surveillance colonoscopy. This ulceration in the ascending colon revealed adenocarcinoma. This patient subsequently underwent total colectomy with ileostomy. 

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... repair genes (eg, hMLH1, hMSH2 ) and p16, leads to methylation- induced silencing. The p27 protein, which binds and prevents both the activation of cyclin E-CDK2 or cyclin D-CDK4 complexes and the progression of G1-S, is often lost in ulcerative colitis– colorectal cancer. 36 , 37 The identification of essential regulatory factors and crucial events in the development of IBD-CRC has had a significant effect on the understanding of the disease, specifically its progression as it correlates with inflammation and genetic mutation. However, changes in the frequency and timing of these mutational abnormalities continue to pose many unanswered ques- tions. The ability to monitor these changes both clinically and in the laboratory provides medical scientists with the possibility of further delineating a clear pathobiologic cause of IBD-associated neoplasia and rea- soning for such an inversion from sporadic colorectal cancer. Through careful investi- gation of these abnormalities, medical scientists hold the ability to develop novel screening techniques and new therapeutic advances. The goal of colorectal cancer screening colonoscopy in the general population and surveillance in IBD patients is to detect premalignant changes early enough that intervention can prevent complications of invasive cancer. The intervention man- dated in IBD-associated dysplasia is colectomy, because of the high prevalence of synchronous or metachronous cancer, as well as the technical limitations of being able to identify confidently and completely resect dysplastic lesions in flat mucosa. In the general population, the dysplastic or premalignant lesion is the colon polyp that can be easily visualized and resected at the time of the colonoscopy before it transforms into a malignant lesion. In contrast, dysplasia in IBD can be found at distant sites from the cancer itself or before the cancer develops and is difficult to rec- ognize on colonoscopy, as it often arises from flat, normal-appearing mucosa (Figure 2). 38 Dysplasia can also occur within or near plaque-like lesions or raised polypoid masses, defined as dysplasia-associated lesion or mass (DALM). Because IBD-CRC is preceded by dysplasia, finding dysplasia on random colon biopsies represents an increased risk of developing colorectal cancer in the near future. Dysplasia is classi- fied as indefinite, low-grade, and high- grade. IBD-CRC occurs in areas of chronic inflammation and can be a polypoid, ulcer- ated, or plaque-like lesion. Most IBD-CRCs are adenocarcinoma, but there is a higher incidence of poorly differentiated, anaplas- tic, and mucinous carcinomas compared with sporadic colorectal cancer. In a comprehensive review of 10 studies of dysplasia surveillance that included a total of 1225 patients with ulcerative colitis, the likelihood of finding concurrent colon cancer at the time of colectomy in patients with high- or low-grade dysplasia was 42% and 19%, respectively. 39 Although prophylactic proctocolectomy can essentially elim- inate the risk of cancer, most patients and their physicians opt for a lifelong program of surveillance. This entails regular medical follow-up, management with anti-inflammatory and potentially chemopreventive agents, as well as periodic colonoscopic examinations combined with extensive biopsy sampling throughout the colon. Although a surveillance program is the best approach currently available, it has its limitations. Surveillance cannot guarantee against the development of colorectal cancer. It is important for both the patient and the physician to understand the risks of potentially missed lesions and the benefits of a strict surveillance program. Physician compliance in adhering to the surveillance biopsy recommendations is important. There should be regular call-back for all participat- ing patients so that no patients are lost to follow-up. Patient noncompliance should trig- ger a series of letters, including a comment about the potential risk for developing colorectal cancer in the absence of follow-up. 40 Based on previous epidemiologic data, guidelines from the Crohn’s and Colitis Foundation of America (CCFA) 40 and, more recently, from the European Crohn’s and Colitis Organisation (ECCO) 41 suggest a relatively strict surveillance policy. The American Gastroenterology Association (AGA) and most other gastrointestinal associations conclude that the risk of colorectal cancer–associated Crohn’s colitis is similar to that of ulcerative colitis for comparable extent, duration, and age of onset of inflammatory disease. As a result, the surveillance strategy for ulcerative colitis also ap- plies for Crohn’s colitis. The recommended guidelines are as follows: 40 – 44 ● Screening colonoscopy should be performed when the disease is in remission. ● Initial surveillance colonoscopy should be performed in each patient beginning 8 –10 years after symptom onset, partly to reassess disease extent. ● Regular surveillance should begin on an annual or biannual basis beginning 8 –10 years of disease for patients with left-sided or extensive colitis after symptom onset. 43 , 44 There should be a decrease in the screening interval with increasing disease duration (from every other year to yearly). Patients with proctosigmoiditis, who have little or no increased risk of colorectal cancer compared with the general population, should be managed according to standard colorectal cancer prevention measures. ● Patients with PSC represent a sub- group of IBD patients at higher risk for IBD-CRC, thus surveillance should be performed annually from the time of PSC diagnosis. ● Two to four random biopsy specimens should be taken every 10 cm from the entire colon, with additional samples of suspicious areas. Particularly in ulcerative colitis, consideration should be given to taking 4-quadrant biopsies every 5 cm in the lower sigmoid and rectum, because the frequency of colorectal cancer is higher in this region. Random biopsies visualize only 1% of total colonic mucosa surface area, promot- ing a high sampling error. In a retrospective review, the probability of detecting dysplasia was 90% if 33 and 95% if 56 random biopsies were taken. 45 The cost of additional random biopsies to the current recommended 33 is hard to justify. 13 To help increase the detection yield of random biopsies, jumbo biopsies can be used. In a prospective study by Elmunzer et al, 46 jumbo forceps were found to be superior to standard large-capacity forceps in obtaining diagnostically adequate surveillance biopsy specimens. One problem with this study was the high interobserver variability between pathologists in analyzing the spec- imen. Nevertheless, jumbo biopsy forceps are recommended as part of colorectal cancer surveillance. Targeted biopsies are an attractive alterna- tive to random biopsies to increase the yield of dysplasia detection. Chromoendoscopy uses a dye sprayed on the colonic mucosa to enhance the visualization of subtle mucosal changes ...