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作 者:陈立新[1] 杨少波[1] 吴志强[1] 唐晓兰[1]
机构地区:[1]解放军第304医院
出 处:《解放军医学杂志》1999年第3期206-207,共2页Medical Journal of Chinese People's Liberation Army
摘 要:为探讨癌相关基因与幽门螺杆菌(HP)感染在胃粘膜病变中有无相互作用关系,随机对136例胃镜检查的慢性浅表性胃炎、慢性萎缩性胃炎、胃溃疡、胃癌患者的胃粘膜活检进行了癌相关基因ras、p16、p53及HP检测。结果显示ras、p16及p53在胃癌的阳性表达均高于胃炎和胃溃疡,经统计学处理除ras(P<0.05)外差异均无显著性意义,HP阳性的胃癌中,ras和p53阳性表达均高于胃炎和胃溃疡,而p16的阳性表达则低于胃炎;ras、p16、p53、HP阳性者和HP阳性的ras、p16、p53阳性表达在萎缩性胃炎伴有肠上皮化生(或)和非典型增生的均高于阴性者,差异有显著性意义(P<0.05),显示癌相关基因和HP感染在胃粘膜的组织学变化中起一定作用并可能有相互作用。To probe the relation between oncogene and Helicobacter pylori (HP) infection in gastric mucosa lesions, ras, p16, p53 and HP were randomly determined in the mucosa biopsies of 136 patients with chronic superficial gastritis, chronic atrophic gastritis, gastric ulcer and gastric cancer diagnosed by gastroscopy. The results showed that the positive rates of ras in gastric cancer were much higher (P<0.05) than that in gastritis and gastric ulcer, and p16 lower than that in gastritis. The positive expressions of ras, p16, p53, HP, and HPpositive ras, p16 and p53 were much higher (P<0.05) than those of negative expression in chronic atrophic gastritis concomitant with intestinal metaplasia and/or a typical hyperplasia. It was suggested that oncogene and HP infection played a role in histological changes and might have an interactive relation.
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