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目的 (1)探讨幽门螺杆菌 (Hp)与胃腺癌的相关性 ,特别是 cag A因子与胃腺癌相关性 ;(2 )探讨 Hp特别是 cag A因子与胃粘膜中 Bcl- 2、Bax、P2 1 - WAF 1 、P1 6 - MTS1 蛋白表达异常的关系 ,从而探讨 cag A是否为一致癌因子及其致癌的可能机理 ;(3)通过对胃腺癌演化系列胃粘膜中 Bcl- 2、Bax、P2 1 - WAF1 、P1 6 - MTS1 蛋白的检测 ,探讨胃腺癌发生的可能机制。 方法 (1)利用血抗 Hp-Ig G、RU T、PCR- Hp- DNA3种方法检测 2 70例病人耳垂血或胃粘膜活检组织中的 Hp及其 cag A基因 ;(2 )利用免疫组化 S- P法检测胃癌演化系列胃粘膜中 Bcl- 2、Bax、P2 1 - WAF 1 、P1 6 - MTS1 蛋白的表达 ;(3)利用 SPSS统计软件包作统计学分析处理。 结果 (1)福州地区 Hp感染率 6 8.2 5 % ,男性 cag A+Hp感染率为 6 3.41% ,女性为 41.94% ;cag A+Hp致胃炎程度及活动性均较cag A - Hp及 Hp者高 (P<0 .0 5 ) ;男性感染 cag A +Hp更易发展为 CAG、IM(P<0 .0 5 ) ;感染 Hp者胃腺癌的分化程度低 ,且向周围浸润及淋巴结转移的能力强 (P<0 .0 5 ) ,但与 cag A因子无关 (P>0 .0 5 ) ;非贲门腺癌患者血抗 Hp- Ig G抗体为 76 .32 % ,大于贲门癌 (5 2 .90 % ) (P<0 .0 5 )。 (2 )在 CSG、CAG、IM阶段 ,Hp感染促进胃粘膜中
Objective (1) To investigate the correlation between Helicobacter pylori (Hp) and gastric adenocarcinoma, especially the correlation between cag A and gastric adenocarcinoma. (2) To investigate the relationship between Hp, especially cag A and Bcl-2, Bax, 1 - WAF 1 and P1 6 - MTS1 in gastric mucosa, so as to investigate whether cag A is a consensus carcinogen and its possible mechanism of carcinogenesis. (3) 1 - WAF1, P1 6 - MTS1 protein in gastric cancer and explore the possible mechanism of gastric adenocarcinoma. Methods (1) Blood Hp-Ig G, RU T and PCR-Hp-DNA were used to detect Hp and its cag A gene in the blood vessels of the ear lobe or gastric mucosa of 2 70 patients. (2) The expressions of Bcl-2, Bax, P2 1 - WAF 1 and P1 6 - MTS1 in gastric cancer gastric mucosa were detected by S-P method. (3) SPSS statistical package was used for statistical analysis. Results (1) The infection rate of Hp in Fuzhou was 6 8.25%, the infection rate of cag A + Hp in male was 6 3.41% and that of female was 41.94%. The degree and activity of gastritis induced by cag A + Hp were higher than those of cag A - Hp and Hp (P <0.05). The infection of cag A + Hp in male was more likely to be CAG, IM (P <0.05). The ability of Hp infected patients to differentiate into gastric adenocarcinoma with low degree of differentiation and infiltration and lymph node metastasis (P <0.05), but no correlation with cag A (P> 0.05). The blood anti-Hp-Ig G antibody in non-cardiac adenocarcinoma was 76.32% 90%) (P <0.05). (2) In the CSG, CAG, IM stage, Hp infection promotes gastric mucosa