幽门螺杆菌在胃癌发生过程中的作用机制

目的：探讨脚可能的致癌机制．方法：采用Warthin—Starry嗜银染色法检测胃癌组织39例，胃黏膜不典型增生24例和慢性胃炎组织33例中的却感染情况；采用PCR法检测上述标本中HpcagA；采用免疫组化S-P法检测组织中iNOS，VEGF，c—erbB-2和ras癌基因产物p185和p21的表达．结果：Hp，HpcagA，iNOS，VEGF，p185和p21在不典型增生和胃癌组织中的表达显著高于慢性胃炎组织；脚阳性慢性胃炎、不典型增生和胃癌组织中iNOS，VEGF和p21的表达显著高于脚阴性组，却阳性不典型增生及胃癌组织中p185的表达显著高于脚阴性组；慢性胃炎、不典型增生和胃癌组织中却与iNOS，VEGF和p21表达呈正相关，不典型增生和胃癌组织中脚与p185表达呈正相关．结论：脚的致癌作用与其HpcagA的过度表达，增强胃黏膜细胞中iNOS和VEGF的表达，促进胃黏膜细胞癌基因c—erbB-2和ras的活化密切相关．

Role of Helicobacter pylori in development of gastric cancer

AIM: To study the possible carcinogenesis of Helicobacter pylori(Hp) infection in the development of gastric cancer. METHODS: Hp was determined by Warthin-Starry silver staining in 39 samples of gastric cancer tissue, 24 samples of gastric mucosal atypical hyperplasia tissue and 33 samples of chronic gastritis tissue. HpcagA was determined by polymerase chain reaction (PCR) and the expressions of iNOS, VEGF, p185 and p21 were examined by S-P immunohistochemical staining. RESULTS: The expressions of Hp, HpcagA, iNOS, VEGF, p185 and p21 in gastric mucosal atypical hyperplasia and gastric cancer tissue were significantly higher than those in chronic gastritis. The expressions of iNOS, VEGF and p21 in Hp positive chronic gastritis, gastric mucosal atypical hyperplasia and gastric cancer cases were significantly higher than those in Hp negative cases. The expression of p185 in Hp positive gastric mucosal atypical hyperplasia and gastric cancer cases was significantly higher than that in Hp negative cases. The expression of Hp was positively related with iNOS, VEGF and p21 in chronic gastritis, gastric mucosal atypical hyperplasia and gastric cancer cases. The expression of Hp was positively related with p185 in gastric mucosal atypical hyperplasia and gastric cancer cases. CONCLUSION: Hp infection leads to the overexpression of HpcagA, iNOS and VEGF, which can stimulate the higher expressions of oncogene c-erbB-2 and ras. It may be one of the crucial mechanisms of induction of gastric cancer by Hp.