胃癌组织PTEN、cyclinE表达与幽门螺旋杆菌感染的关系

Relationship between expression of PTEN and cyclinE and Helicobacter pylori infection in gastric cancer

目的:探讨胃癌及癌旁组织中H pylori感染和PTEN、cyclinE表达,他们之间的相关性以及胃癌发生的可能机制. 方法:每例标本采用快速尿素酶试验,组织病理学检测两种方法检查H pylori,采用免疫组化法检测胃癌组织及癌旁组织59例中PTEN及cyclinE的表达. 结果:胃癌组织PTEN在阳性率明显低于癌旁组织,二者之间有显著差异(50.85%VS 96.61%P<0.05);胃癌组织cyclinE阳性率高于癌旁组织,二者之间有显著差异(55.93%vs 40.7%P>0.05);PTEN在高中分化腺癌中的表达率明显高于低分化腺癌和黏液癌,有显著差异(68.4%vs 33.3%P<0.05,68.4%vs 37.5%,P<0.05);胃黏液癌及低分化腺癌CyclinE阳性表达明显高于高中分化腺癌,有显著差异(68.8%vs 3 1.5%P<0.05,66.7% vs 31.5%,P<0.05);H pylori性的PIEN阳性表达率明显低于H pylori阴性,二者之间有显著差异(24.2%vs69.2% P<0.05);cyclinE表达阳性率在Hpylon阳性和阴性胃癌中,二者之间无显著差异(51.9%vs59.4%P>0.051. 结论:胃癌的发生与抑癌基因PTEN的下调和癌基因cyclinE的过度表达有关,H pylori感染的致癌机制中可能有抑癌基因PTEN参与.

AIM: To investigate the relationship between H pylori infection and PTEN, cyclinE expression in gastric cancer and adjacent mucosal tissues, and to study the possible mechanism of H pylori in gastric carcinogenesis. METHODS: Both rapid urease and pathological test were used to examine H pylori in 59 cases of specimen. The expression of PTEN and cydinE in gastric cancer and adjacent mucosal tissues was detected by immunohistochemical technique (SP method). RESULTS: PTEN expression in gastric cancer tissues was significantly lower than that in the cancer adjacent tissues (50.85% vs 96.61%, P<0.05); however, CyclinE expression in gastric cancer tissues was significantly higher than that in cancer adjacent tissues. The level of PTEN expression in well-differentiated adenocarcinoma was significantly higher than that in poorly-differentiated adenocarcinoma and mucinous carcinoma (68.4% vs 333%, P<0.05 68.4% vs 37.5%, P<0.05 respectively); however, the level of CyclinE expression in well-differentiated adenocarcinoma was significantly lower than that in poorly-differentiated adenocarcinoma and mucinous carcinoma (31.5% vs 68.8%, P<0.05; 31.5% vs 66.7%, P<0.05); PTEN expression in in H Pylori positive group was lower than that in H pylori negative group (51.9% vs 559.4%, P>0.05); CyclinE ex pression had no significant difference between H pylori positive and negative gastric cancer tissues. CONCLUSION: Pathogenesis of gastric cancer relates to loss of suppression gene PTEN and over-expression of oncogene cyclinE, and suppression gene PTEN probably plays a role in development of gastric cancer induced by H pylori infection.