论文部分内容阅读
目的研究江苏省胃癌高发区幽门螺杆菌（Ｈｐ）感染及其毒力因子与胃癌、基因突变之间的关系。方法用酶链免疫吸附测定（ＥＬＩＳＡ）、免疫印迹及聚合酶链反应单链构象多态性分析（ＰＣＲＳＳＣＰ）等方法，分析了５０例胃癌及５０例配对胃炎患者的Ｈｐ感染、Ｈｐ的细胞毒素相关蛋白（ＣａｇＡ）、空泡细胞毒素（ＶａｃＡ）情况及胃粘膜ｐ５３基因第５～８外显子的突变。结果胃癌组中Ｈｐ阳性率及ＣａｇＡ阳性率均显著高于胃炎组，ｐ５３基因突变与Ｈｐ感染有非常显著的相关性，而与ＣａｇＡ、ＶａｃＡ的表达无关。结论Ｈｐ（尤其是ＣａｇＡ阳性菌株）感染能增加胃癌的发病风险，在Ｈｐ致癌过程中ｐ５３等基因突变可能起了关键的作用，研究结果为根治Ｈｐ以预防胃癌发生提供了实验依据。
Objective To investigate the relationship between Helicobacter pylori (Hp) infection and its virulence factors and gastric cancer and gene mutations in high-risk areas of gastric cancer in Jiangsu Province. Methods Enzyme-linked immunosorbent assay (ELISA), western blot and polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) were used to analyze Hp infection and Hp in 50 cases of gastric cancer and 50 cases of gastritis. The cytotoxin-associated protein (CagA), vacuolar cytotoxin (VacA) and mutations in exon 5-8 of p53 gene in gastric mucosa. Results The positive rates of Hp and CagA in the gastric cancer group were significantly higher than those in the gastritis group. The p53 gene mutation had a significant correlation with Hp infection, but was not related to the expression of CagA and VacA. Conclusion The infection of Hp (especially CagA positive strains) can increase the risk of gastric cancer. The mutation of p53 gene may play a key role in Hp carcinogenesis. The research results provide experimental basis for the eradication of Hp to prevent the occurrence of gastric cancer.