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Steven H. Itzkowitz, Fingerprinting the Colon?, Inflammatory Bowel Diseases, Volume 9, Issue 5, 1 September 2003, Pages 338–339, https://doi.org/10.1097/00054725-200309000-00009
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DNA fingerprinting abnormalities can distinguish ulcerative colitis patients with dysplasia and cancer from those who are dysplasia/cancer-free. Chen R, Rabinovitch PS, Crispin DA, Emond MJ, Koprowicz KM, Bronner MP, Brentnall TA. Am J Pathol 2003;162:665–72.
Patients with longstanding ulcerative colitis (UC) are at increased risk for developing colorectal cancer. In previous studies, patients with UC who had already developed dysplasia or cancer were found to have widespread genomic instability in their colonic mucosa, even in areas that were not dysplastic. To further examine genomic instability in the colons of patients with UC, the authors used two sensitive polymerase chain reaction (PCR)–based techniques to create DNA “fingerprints” of the colon. The intersimple sequence repeat PCR (ISSR-PCR) and arbitrarily primed PCR (AP-PCR) techniques use random primers to amplify the genome. Both of these methods were applied to DNA extracted from colonic epithelial cells isolated from tissue representing various histologic grades of dysplasia or cancer. The PCR products are run on a gel, producing a pattern (“fingerprint”) of bands, which is then compared with that of matched constitutional stromal tissue from the same patient to detect unique genomic changes associated with neoplasia. The pattern that emerges represents gains or losses of bands in the colonic cells compared with normal stromal cells. Any band with greater than twofold intensity change compared with its constitutional counterpart was scored as a change. The tissue was derived from three groups of patients: 11 UC patients with cancer/dysplasia (termed progressors), 10 UC patients without cancer/dysplasia (termed nonprogressors), and 7 control patients without UC. Among the progressors, 2 patients had cancer as their worst histology, and 9 had dysplasia. The 10 nonprogressors remained dysplasia-free throughout several years of surveillance. There was no substantial difference in disease duration between the progressors and nonprogressors. Specimens from all of the progressors and two nonprogressors were obtained from surgical resections; the remaining specimens from the nonprogressors came from colonoscopic biopsies.
