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作 者:马秀梅[1] 王玉芳[2] 耿丽萍[2] 左连富[1]
机构地区:[1]河北医科大学第四附属医院河北省肿瘤研究所,河北石家庄050011 [2]内蒙古医学院病理教研室,内蒙古呼和浩特010059
出 处:《癌变.畸变.突变》2006年第1期50-53,共4页Carcinogenesis,Teratogenesis & Mutagenesis
摘 要:背景与目的通过检测幽门螺旋杆菌(Helicobacter Pylori,H.pylori)感染胃粘膜组织环氧合酶-2(Cyclooxygenase-2,COX-2)和多药耐药-1(Multidrug resistance-1,MDR-1)基因表达产物P糖蛋白(P-glycoprotein,P-gp)表达,探讨幽门螺旋杆菌相关胃癌的发生机制,以及P-gp高表达的机制。材料与方法慢性胃炎155例(30例慢性浅表性、40例慢性萎缩性、45例肠化、40例非典型增生)及胃癌80例(肠型40例,弥漫型40例),COX-2和P-gp表达检测选择免疫组化S-P法,H.pylori感染检测采用快速脲素酶及改良Giemsa染色方法。结果H.pylori阳性感染率、COX-2和P-gp的阳性表达率,肠型胃癌均明显高于弥漫型胃癌(P<0.01)。慢性萎缩性胃炎、肠化、非典型增生及肠型胃癌中H.pylori感染与COX-2的表达呈正相关(P<0.01)。H.pylori感染的慢性浅表性胃炎、慢性萎缩性胃炎、肠化、非典型增生及肠型胃癌中COX-2的表达与P-gp的表达也均呈正相关(P<0.01)。结论H.pylori依赖的COX-2表达与P-gp表达有关,可能有助于胃癌形成以及胃癌对化疗抵制。BACKGROUND & AIM: To explore the mechanism of Helicobacter Pylori (H.pylori) -related gastric carcinogenesis and overexpression of the multidrug-resistant-1 (MDR-1) gene-encoded P-glycoprotein (P-gp) via examining Cyclooxygenase-2(COX-2) and P-gp expression in the affected gastric mucosa. MATERIAL AND METHODS: 155 chronic gastritis specimens (30 chronic superficial gastritis specimens, 40 chronic atrophic gastritis specimens, 45 intestinal metaplasia specimens, 40 dysplasia specimens) and 80 gastric carcinoma specimens(40 intestinal type and 40 diffuse type) were selected. COX-2 and P-gp expression were detected by immunohistochemistry. H. pylori infection was assessed by rapid urease test and histological examination(modified Giemsa staining) . RESULTS: H.pylori infection rate, COX-2 positive expression rate and P-gp positive expression rate in intestinal-type gastric carcinoma specimens were significantly higher than those in diffuse-type gastric carcinoma specimens(P 〈 0.01). Expression of COX-2 was positively correlated with H.pylori infection in chronic atrophic gastritis, intestinal metaplasia, dysplasia and intestinal-type gastric carcinoma( P 〈 0.01) Expression of COX-2 was positvely correlated with that of P-gp in chronic superficial gastritis, chronic atrophic gastritis, intestinal metaplasia, dysplasia, and intestinal-type gastric carcinoma with H.pylori infection (P 〈 0.01). CONCLUSION: H. pylori-dependent induction of COX-2 was associated with enhanced prodution of P-gp that might contribute to gastric tumourigenesis and resistance to chemotherapy.
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