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目的检测大肠平坦型腺瘤、隆起型腺瘤和浸润性大肠癌p53、c-myc和ki-67的表达水平,探讨其基因调控机制。方法选取2002至2006年间行结肠镜检查并经病理证实的平坦型、隆起型腺瘤和腺癌的病变标本,用免疫组织化学二步法检测p53、c-myc和ki-67的表达水平,分析三者表达水平在各组病变的差异和意义。结果p53、c-myc和ki-67在平坦型腺瘤、隆起型腺瘤和腺癌中阳性表达率分别为3.33%(1/30)、8.06%(5/62)和69.44%(25/35);33.33%(10/30)、58.06%(36/62)和80.56%(29/36);23.33%(7/30)、19.35%(12/62)和50.00%(18/36);在正常组织中均无明显表达。结论平坦型腺瘤、隆起型腺瘤和大肠癌三者具有不同的p53、c-myc和ki-67表达,提示三者的发生、发展可能存在不同基因调控机制,平坦型腺瘤的癌发生途径可能与隆起型腺瘤不同。
Objective To detect the expression of p53, c-myc and ki-67 in colorectal adenoma, adenohypophysis and invasive colorectal carcinoma, and to explore its gene regulatory mechanism. Methods The pathological specimens of colon, adenoma and adenocarcinoma of flat type, elevated type and pathologically confirmed by colonoscopy from 2002 to 2006 were collected. The expressions of p53, c-myc and ki-67 were detected by immunohistochemical two-step method. Analysis of the three levels of expression in the differences between the groups and significance. Results The positive rates of p53, c-myc and ki-67 were 3.33% (1/30), 8.06% (5/62) and 69.44% (25/62) in adenoma, 33.33% (10/30), 58.06% (36/62) and 80.56% (29/36); 23.33% (7/30), 19.35% (12/62) and 50.00% (18/36) ; No obvious expression in normal tissues. Conclusions The expression of p53, c-myc and ki-67 in different types of adenoma, adenoma and colorectal cancer are different, suggesting that there may exist different gene regulatory mechanisms and the occurrence of carcinoma of flat adenoma Pathway may be different from elevated adenoma.