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目的 :探讨胃癌胃粘膜演变过程中各个不同阶段粘膜组织端粒酶表达规律及其与幽门螺杆菌 (HP)感染的关系。方法 :采用端粒酶TPCR ELISA法检测 19例慢性浅表性胃炎 (CSG)、15例胃粘膜肠上皮化生 (ICM )、15例胃粘膜轻度异型增生、14例胃粘膜重度异型增生、2 9例胃腺癌组织端粒酶活性 ,并对其中HP阳性与阴性病变组织的端粒酶阳性率进行对比研究。结果 :端粒酶阳性率由CSG→ICM→胃粘膜轻度异型增生→重度异型增生→胃癌逐渐增高 ,分别为 0、40 0 %、40 0 %、78 6%、79 3 %。胃癌及重度异型增生组与其它各组比较有显著差异 (χ2 =4.44 ,P <0 0 5 )。各组HP感染率分别为CSG 3 1 6%、ICM 73 3 %、胃粘膜轻度异型增生 66 7%、重度异型增生 64 3 %、胃癌 44 8%。ICM及轻度异型增生组与CSG组比较差异显著 (χ2 =5 .85 ,P <0 0 5 )。各病变组织中HP阳性与阴性组间端粒酶阳性表达率无明显差异。结论 :端粒酶激活是胃癌发生的早期事件。HP现行感染与端粒酶阳性表达无明显关系。
Objective: To investigate the expression of telomerase in mucosal tissues and the relationship with Helicobacter pylori (HP) infection in different stages of gastric mucosal gastric mucosa. Methods: Nineteen cases of chronic superficial gastritis (CSG), 15 cases of gastric mucosal intestinal metaplasia (ICM), 15 cases of gastric mucosal mild dysplasia, 14 cases of severe gastric mucosal dysplasia were detected by telomerase TPCR ELISA. The telomerase activity in 29 cases of gastric adenocarcinoma was analyzed, and the positive rate of telomerase in HP positive and negative lesions was compared. Results: The positive rate of telomerase was gradually increased from CSG → ICM → mild gastric dysplasia → severe dysplasia → gastric cancer with 0,40 0%, 40 0%, 78 6% and 79 3%, respectively. Gastric cancer and severe dysplasia group were significantly different from other groups (χ2 = 4.44, P <0.05). The infection rates of HP in each group were CSG166%, ICM73 3%, gastric mucosal mild dysplasia 66.7%, severe dysplasia 64.3% and gastric cancer 44.8%. There was significant difference between ICM and mild dysplasia group and CSG group (χ2 = 5.85, P <0.05). There was no significant difference in the positive rate of telomerase between HP positive and negative groups in all lesions. Conclusion: Telomerase activation is an early event in gastric cancer. There is no significant relationship between the current infection of HP and the positive expression of telomerase.