Dysplasia and Cancer in Inflammatory Bowle Disease, An Issue by Gastroenterology Clinics of North America PDF

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Inactivation occurs typically by two separate mechanisms; allelic deletion (LOH) of one allele and mutation of the other. The classic tumor suppressor genes APC, p53, and DCC/DPC4, which are important for sporadic colon carcinogenesis, have also been implicated in CAC. APC tumor suppressor gene As noted previously, APC mutations are rare in UC and occur late in the progression from dysplasia to carcinoma (see Fig. 1). Mutations in APC are rarely if ever encountered in colitic mucosa that is negative or indefinite for dysplasia [25], and fewer than 14% of tissues manifesting LGD harbor APC mutations [25,49].

J Biol Chem 2000;275:20887–95. [64] Jiang Z, Woda BA, Rock KL, et al. P504S: a new molecular marker for the detection of prostate carcinoma. Am J Surg Pathol 2001;25:1397–404. [65] Jiang Z, Fanger GR, Woda BA, et al. Expression of alpha-methylacyl-CoA racemase (P504s) in various malignant neoplasms and normal tissues: a study of 761 cases. Hum Pathol 2003;34:792–6. [66] Odze RD, Farraye FA, Hecht JL, et al. Long-term follow-up after polypectomy treatment for adenoma-like dysplastic lesions in ulcerative colitis.

81] Delaunoit T, Limburg PJ, Goldberg RM, et al. Colorectal cancer prognosis among patients with inflammatory bowel disease. Clin Gastroenterol Hepatol 2006;4:335–42. [82] Sugita A, Greenstein AJ, Ribeiro MB, et al. Survival with colorectal cancer in ulcerative colitis. A study of 102 cases. Ann Surg 1993;218:189–95. [83] Greenstein AJ, Slater G, Heimann TM, et al. A comparison of multiple synchronous colorectal cancer in ulcerative colitis, familial polyposis coli, and de novo cancer. Ann Surg 1986;203:123–8.

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Dysplasia and Cancer in Inflammatory Bowle Disease, An Issue of Gastroenterology Clinics by Gastroenterology Clinics of North America


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