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目的：探讨幽门螺杆菌（Ｈｐ）感染与ｒａｓ原癌基因产物ｐ２１（ｒａｓｐ２１）蛋白和ｐ５３癌基因产物突变型ｐ５３蛋白表达的关系。方法：应用免疫组织化学方法，检测慢性浅表性胃炎（ＣＳＧ）３０例、胃粘膜不全结肠型肠化生（ＩＣＭ）２５例、异型增生２９例、胃癌３７例的活检标本。结果：ＩＣＭ组、异型增生组和胃癌组的Ｈｐ感染率均明显高于ＣＳＧ组（Ｐ＜０．０５）。ｒａｓｐ２１及突变型ｐ５３蛋白的阳性表达率在ＣＳＧ组均为０，而在异型增生组和ＩＣＭ组的表达均明显低于胃癌组（４５％和３８％、３２％和３２％对６０％和７０％），Ｐ＜０．０５，Ｐ＜０．０１；其中胃癌、异型增生及ＩＣＭ组中的Ｈｐ阳性组的ｒａｓｐ２１及突变型ｐ５３蛋白表达阳性率均明显高于Ｈｐ阴性组（Ｐ＜０．０５或Ｐ＜０．０１）。经根除Ｈｐ治疗后，Ｈｐ根除者的ｒａｓｐ２１及突变型ｐ５３蛋白表达由阳性转为阴性的例数比Ｈｐ未根除者多（Ｐ＜０．０５，Ｐ＜０．０１）。结论：Ｈｐ感染可能参与了ｒａｓ癌基因的激活和ｐ５３抑癌基因的突变，这可能是其致癌机制之一。
Objective: To investigate the relationship between Helicobacter pylori (Hp) infection and expression of ras proto-oncogene product p21 (rasp21) protein and p53 oncogene product mutant p53 protein. METHODS: Immunohistochemistry was used to detect 30 cases of chronic superficial gastritis (CSG), 25 cases of gastric incomplete intestinal metaplasia (ICM), 29 cases of dysplasia, and 37 cases of gastric cancer. Results: The Hp infection rate in ICM group, dysplasia group, and gastric cancer group was significantly higher than that in CSG group (P<0.05). The positive expression rates of rasp21 and mutant p53 protein were all 0 in CSG group, but significantly lower in the dysplasia group and ICM group than in the gastric cancer group (45% and 38%, 32% and 32% vs. 60% and 70) (%), P <0.05, P <0.01; The positive rate of expression of rasp21 and mutant p53 protein in Hp-positive group of gastric cancer, dysplasia and ICM group were significantly higher than that of Hp-negative group (P <0. 05 or P<0.01). After eradication of Hp treatment, the number of positive and negative p53 protein expressions from Hp eradication was significantly higher than that of Hp eradication (P<0.05, P<0.01). Conclusion: Hp infection may be involved in the activation of ras oncogene and mutation of p53 tumor suppressor gene, which may be one of its carcinogenic mechanisms.