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目的 探讨幽门螺杆菌(Hp)感染与胃癌组织p16基因变异的关系。方法 43例胃癌患者的新鲜癌手术标本、相应的癌旁正常组织及血清标本为本组研究对象。分别采用PCR及银染PCR-SSCP技术检测胃癌组织p16基因的纯合性缺失及突变情况;幽门螺杆菌感染状况通过PCR及血清学试验确定。结果 (1)43例胃癌中,Hp阳性30例,阳性率为69.77%,其中CagA阳性24例,阳性率为80%。(2)30例Hp阳性胃癌中,有12例发生p16基因变异,发生率为40%;13例Hp阴性胃癌中,4例p16基因发生变异,发生率为30.77%。Hp阳性组与阴性组相比较p16基因变异率差异无显著性(P>0.05)。(3)30例Hp阳性胃癌中,CagA阳性与阴性组p16基因变异率分别为41 67%(10/24)及33.33%(2/6),两组变异率比较差异无显著性(P>0.05)。结论Hp及CagA阳性Hp感染与胃癌组织p16基因变异无显著相关性,Hp感染可能不是其改变的唯一或必须因素。“,”Objective To investigate the relationship between Helicobacter pylori(H. pylori) in-fection and variation of p16 gene in gastric cancer. Methods The carcinomatous tissues and the normal tissues neighboring carcinoma and serum samples of 43 patients with gastric cancer were studied. The ho-mozygous deletions of p16 gene and the mutations were assessed by PCR and silver stain PCR-SSCP, re-spectively. The status of H. pylori infection was determined by PCR and serological tests. Results (1) In the 43 patients with gastric cancer, H. pylori infection was confirmed in the 30 patients and the positive rate was 69.77%; among these 30 patients, CagA+ H. pylori infection was found in 24 cases (80%).(2)Among the 30 gastric carcinomas with H. pylori infection, 12(40%)presented with variations of p16 gene and among the 13 gastric carcinomas without H. pylori infection, 4 (30.77%) showed the varia-tions of p16 gene without statistical difference ( P>0.05). (3)The variant rate of p16 gene in CagA positive and negative groups was 41.67% (10/24) and 33.33% (2/6) respectively in the 30 patients with H. pylori infection without significant difference ( P>0.05). Conclusions H. pylori and CagA+ H. pylori infection, may not be significantly associated with the variations of p16 gene in gastric cancer and it may not be the single or essential factor for the changing of the gene.