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幽門螺桿菌在胃癌發(fā)生過程中的作用機制
作者：佟書娟，劉亞平，楊丹丹【關鍵詞】 胃腫瘤
Role of Helicobacter pylori in development of gastric cancer
【Abstract】 AIM: To study the possible carcinogenesis of Helicobacter pylori(Hp) infection in the development of gastric cancer. METHODS: Hp was determined by WarthinStarry 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 SP 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 cerbB2 and ras. It may be one of the crucial mechanisms of induction of gastric cancer by Hp.
【Keywords】 stomach neoplasms; vascular endothelial growth factors; nitric oxide synthase; oncogene; helicobacter pylori; cytotoxin associated gene
【摘要】 目的： 探討Hp可能的致癌機制. 方法： 采用WarthinStarry嗜銀染色法檢測胃癌組織39例，胃黏膜不典型增生24例和慢性胃炎組織33例中的Hp感染情況；采用PCR法檢測上述標本中HpcagA；采用免疫組化SP法檢測組織中iNOS, VEGF, cerbB2和ras癌基因產(chǎn)物p185和p21的表達. 結(jié)果： Hp, HpcagA, iNOS, VEGF, p185和p21在不典型增生和胃癌組織中的表達顯著高于慢性胃炎組織；Hp陽性慢性胃炎、不典型增生和胃癌組織中iNOS, VEGF和p21的表達顯著高于Hp陰性組，Hp陽性不典型增生及胃癌組織中p185的表達顯著高于Hp陰性組；慢性胃炎、不典型增生和胃癌組織中Hp與iNOS，VEGF和p21表達呈正相關，不典型增生和胃癌組織中Hp與p185表達呈正相關. 結(jié)論： Hp的致癌作用與其HpcagA的過度表達，增強胃黏膜細胞中iNOS和VEGF的表達，促進胃黏膜細胞癌基因cerbB2和ras的活化密切相關.
【關鍵詞】 胃腫瘤；血管內(nèi)皮生長因子類；一氧化氮合酶；癌基因；螺桿菌，幽門；細胞毒素相關基因
0引言
幽門螺桿菌（Helicobacter pylori, Hp）感染與胃癌的發(fā)生發(fā)展密切相關［1，2］，但Hp確切的致癌機制尚不清楚. 我們通過對慢性胃炎、胃黏膜不典型增生及胃癌組織中Hp和細胞毒素相關基因（cytotoxin associated gene A, cagA）陽性株感染率，誘導型一氧化氮合酶（inducible NOS, iNOS），血管內(nèi)皮生長因子（vascular endothelial growth factor, VEGF），cerbB2和ras癌基因產(chǎn)物p185和p21蛋白表達情況及Hp與iNOS, VEGF, p185和
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