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胃黏膜癌变过程中幽门螺杆菌感染与hTERT及c-myc蛋白的关系 被引量:3

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摘要 幽门螺杆菌(Helicobacter pylori,H.pylor)感染是慢性胃炎的主要病因之一,与胃癌的发生密切相关.H.pylori感染致癌的确切机制目前尚不清楚.众多研究表明,端粒酶激活与肿瘤的发生、发展密切相关.端粒酶逆转录酶(human telomerase reverse transcriptase,hTERT)是端粒酶活性的必需和限速成分,其基因表达水平与细胞端粒酶活性的表达一致[1,2].c-myc蛋白是由myc原癌基因编码的一种转录因子,有研究表明c-myc可致hTERT基因表达上调从而使端粒酶激活[3].我们采用免疫组织化学法检测胃黏膜癌变过程中H.pylori阳性及H.pylori阴性胃黏膜组织中hTERT及c-myc蛋白的表达,旨在探讨H.pylori感染可能的致癌机制.
机构地区 江西医学院
出处 《现代消化及介入诊疗》 2003年第1期35-37,共3页 Modern Interventional Diagnosis and Treatment in Gastroenterology
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