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胃黏膜肠化生表型转变机制的研究进展

Research progress of pathogenesis of phenotype shift of gastric intestinal metaplasia
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摘要 胃黏膜肠化生是临床常见的病理学诊断,是肠型胃癌的癌前病变,其发病机制目前还不清楚,主要与幽门螺杆菌(Hp)感染、胆汁反流、亚硝酸盐的摄入及维生素缺乏等有关。研究发现,胃上皮向肠上皮转分化所涉及的相关基因有CDX2、SOX2、PDX1、OCT1、SHH、Runx3、Tff等。总之,胃黏膜肠化生表型转变是一个复杂且漫长的过程,目前针对其病因如Hp感染、胆汁反流等的治疗仅能控制其进展而未能反转其临床过程,仍需深入探明其发病机制,以指导临床治疗。 Gastric intestinal metaplasia (IM), a common clinical pathological diagnosis, is a premalignant condition of intestinal type gastric cancer. The pathogenesis is still unclear, which links with helicobacter pylori (Hp) infection, bile reflux, nitrite intake, vitamin deficiency and so on. In recent studies, the relevant genes involved with transdifferentiation of gastric epithelium to intestinal epithelium are CDX2, SOX2, PDX1, OCT1, SHH, Runx3, Tff, and so on. Overall, the phenotype shift of gastric intestinal metaplasia is a complex and long process, current treatments targeted to the cause of IM such as Hp infection, bile reflux only can prevent its development, but fail to reverse the clinical process, so further clarification to the pathogenesis is still needed to guide the clinical treatment.
出处 《肿瘤研究与临床》 CAS 2015年第9期640-642,共3页 Cancer Research and Clinic
关键词 胃黏膜肠化生 表型转变 机制 Gastric intestinal metaplasia Phenotype shift Pathogenesis
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