机构地区:[1]徐州医学院附属第三医院消化科,江苏省徐州市221003 [2]徐州医学院附属第三医院病理科,江苏省徐州市221003
出 处:《世界华人消化杂志》2011年第6期596-601,共6页World Chinese Journal of Digestology
基 金:江苏省徐州市科技计划基金资助项目;No. XM08C067~~
摘 要:目的:探讨染色放大内镜下大肠病变的腺管开口分型与病变组织hMLH1和hMSH2蛋白表达的关系.方法:根据Kudo分型方法,染色放大内镜下大肠病变腺管开口分为Ⅰ-Ⅴ型;所有病灶性质由病理组织学分别确诊为非肿瘤性病变、腺瘤性病变及癌性病变;免疫组织化学方法检测活检组织hMLH1和hMSH2蛋白的表达.结果:应用染色放大内镜对146例患者的大肠黏膜进行细微结构形态学观察,共检出息肉样病变256枚.随着腺管开口分型序数的递增,活检组织中hMLH1与hMSH2蛋白的丢失率逐渐增高,Ⅰ-Ⅴ型hMLH1丢失率分别为0.00%(0/11)、1.61%(1/62)、19.68%(25/127)、33.33%(1/3)、32.26%(10/31)、36.36%(8/22);hMSH2蛋白丢失率分别为0.00%(0/11)、3.22%(2/62)、16.53%(21/127)、33.33%(1/3)、35.48%(11/31)、40.90%(9/22),组间两两比较差异有统计学意义(均P<0.01);74例大肠黏膜非肿瘤性病变中2例hMLH1表达阴性,占2.70%(2/74),3例hMSH2表达阴性,占4.05%(3/74);130例腺瘤组织中30例hMLH1表达阴性,占23.07%(30/130),22例hMSH2表达阴性,占16.92%(22/130);52例癌变组织中13例hMLH1表达阴性,占25%(13/52),16例hMSH2表达阴性,占30.76%(16/52),癌性病变组hMLH1与hMSH2蛋白的丢失率明显高于腺瘤性病变组及非肿瘤性病变组(均P<0.01);hMSH2与hMLH1蛋白的丢失率在不同病变组织中(非肿瘤性病变、腺瘤性病变及癌性病变)无相关性(均P>0.05).结论:随着大肠腺管分型序数的递增,hMLH1和hMSH2蛋白的丢失率逐渐增加,与大肠病变病理诊断中的丢失率具有一致性,提示DNA错配修复基因突变或功能缺失可能是大肠发生癌变进程中的早期事件,染色放大内镜下随访大肠腺管组织中hMLH1和hMSH2蛋白的丢失率有助于发现癌前病变、大肠癌.AIM:To explore the relationship between pit patterns of colorectal polypoid lesions classif ied by magnifying chromoendoscopy and expression of human MutL homolog 1/2(hMLH1/2) proteins in colorectal mucosa.METHODS:Colorectal lesions in 146 patients were classified as type I to V pit patterns by magnifying chromoendoscopy using the Kudo criteria.All lesions were pathologically confirmed as nonneoplastic,adenomatous or cancerous lesions.Colorectal mucosal biopsy specimens were used to detect the expression of hMLH1 and hMSH2 proteins by immunohistochemistry.RESULTS:A total of 256 polypoid lesions were found in 146 patients by magnifying chromoendoscopy.The rates of loss of hMLH1 and hMSH2 protein expression increased gradually from type Ⅰ to type V pit patterns in 256 polypoid lesions [hMLH1:0.0%(0/11),1.61%(1/62),19.68%(25/127),33.33%(1/3),32.26%(10/31),36.36%(8/22);hMSH2:0.00%(0/11),3.22%(2/62),16.53%(21/127),33.33%(1/3),35.48%(11/31),40.90%(9/22);all P 0.01].The rates of loss of hMLH1 and hMSH2 expression were 2.70% and 4.05% in nonneoplastic lesions,23.07% and 16.92% in adenoma lesions,and 25% and 30.76% in cancerous lesions.The rates of loss of hMLH1 and hMSH2 protein expression were signif icantly higher in cancerous lesions than in adenomatous and nonneoplastic lesions(both P 0.01).There was no signif icant difference between the rate of loss of hMLH1 and that of hMSH2 protein expression in all lesions(all P 0.05).CONCLUSION:The rates of loss of hMLH1 and hMSH2 protein expression gradually increased from type Ⅰ to type V pit patterns,suggesting that mutation or functional deficiency of DNA mismatch repair genes is an early event in colorectal carcinogenesis.Lesion classification by magnifying chromoendoscopy or detection of the loss of hMLH1 and hMSH2 protein expression can help identify precancerous and colorectal lesions from colorectal lesions.
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