机构地区:[1]中国医科大学肿瘤研究所第三研究室,辽宁沈阳110001
出 处:《中国癌症杂志》2000年第6期485-488,共4页China Oncology
基 金:国家"九五"攻关课题! ( 96 90 6 0 1 0 4)
摘 要:目的 :研究幽门螺杆菌 (Hp)感染与胃癌的关系及其可能的致癌机制。方法 :利用DNEL技术和免疫组化染色对 10 0例胃粘膜活检组织 ,其中包括正常胃粘膜、Hp阴性和Hp阳性胃癌前各阶段病变及胃癌组织 ,进行细胞凋亡和增殖状态以及P5 3基因表达的分析。结果 :在正常胃粘膜 ,凋亡细胞散布于表层上皮 ,增殖细胞局限于粘膜腺体颈部 ,P5 3蛋白未见表达 ;在胃癌组织 ,凋亡细胞仅占 1 6 2 % ,增殖细胞则占 41 99% ,P5 3蛋白表达明显增强。在肠上皮化生阶段 ,Hp阳性组的凋亡指数、增殖指数和P5 3蛋白表达阳性率均显著高于正常胃粘膜 (P <0 0 1) ;Hp阳性组的凋亡指数高于Hp阴性组 ,Hp阳性组的增殖指数和P5 3蛋白阳性率显著高于Hp阴性组 (P <0 0 1,P <0 0 5 )。而在异型增生阶段 ,Hp阳性组的凋亡指数、增殖指数和P5 3蛋白表达阳性率分别低于阴性组 ,显著高于阴性组 (P <0 0 1)和高于阴性组。在肠上皮化生、异型增生和胃癌组织中 ,Hp阳性组的凋亡指数分别为4 36 % (± 1 95 % )、2 31% (± 1 10 % )、1 34 % (± 0 6 9% ) ,呈明显递减 (P <0 0 1) ;增殖指数分别为 19 11% (±6 79% )、33 89% (± 11 6 5 % )、48 2 7% (± 15 6 7% ) ,呈明显递增 (P <0 0 5或 0 0 1) ;P5 3蛋白表达阳性率呈递增趋势。结论Purpose:To investigate the relationship between HELICOBACTER PYLORI (Hp) and gastric carcinoma, as well as the possible carcinogenic mechanism by Hp. Methods: DNEL technique and immunohistochemical staining were used in the research to study the state of apoptosis, proliferation and p53 gene expression. Total 100 gastric mucosal biopsy specimens, including normal mucosa, Hp negative and Hp positive gastric precancerous lesions as well as gastric carcinomas were studied. Results:There were several apoptotic cells in the superficial epithelium and a few proliferative cells within neck of gastric glands, and no p53 protein expression in normal mucosa. In gastric carcinoma, apoptotic cells accounted for 1.62%, while proliferative cells 4.99%, and P53 protein significantly increased. in metaplasia, the apoptotic index (AI), proliferative index (PI) and positivity of p53 expression in Hp positive group were higher than those in normal mucosa ( P <0.01). AI in Hp positive group was higher than that in Hp negative one. PI and positivity of p53 expression in Hp positive group were higher than those in Hp negative one ( P <0 01 and 0.05). While in dysplasia, AI, PI and positivity of p53 expression in Hp positive group were lower, significantly higher ( P <0 01) and higher than those in Hp negative one respectively. In metaplasia, dysplasia and gastric carcinoma, in Hp positive group, AIs were 4.36%(±1 95%),2 31%(±1 10%) and 1.34%(±0 69%) respectively, with an evident, gradual decrease trend, gradual decrease trend ( P <0 01), and PIs were 19.11% (±6.79%), 33.89% (±11.65%) and 48.27% (±15 67%) respectively, with an evident trend, of gradual increase ( P <0.05 or 0.01),and there was also a trend of gradual increase in positivity of p53 gene expression. Conclusions:It is suggested that in course of the formation of gastric carcinoma, Hp causes proliferation to increase, and in metaplasia Hp induces apoptosis, but in dysplasia Hp inhibits apoptosis. Hp infection strengthens the mutated p5
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