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胃粘膜癌变过程中幽门螺杆菌感染与p53,c-erbB-2基因表达的研究 被引量:49

Study on Helicobacter pylori infection and p53 , c erbB 2 gene expression in carcinogenesis of gastric mucosa
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摘要 目的探讨胃粘膜癌变过程中幽门螺杆菌(Helicobacterpylori,Hp)感染与p53,cerbB2基因表达的关系.方法浅表性胃炎16例,肠上皮化生22例,异型增生14例,早期胃癌18例及进展期胃癌40例作为研究对象.用WarthinStary银染色法检测Hp,用免疫组化Sp法检测p53和cerbB2的基因表达产物.结果Hp,p53,cerbB2在浅表性胃炎的检出率各为500%,00%,00%;在肠上皮化生的检出率各为591%,227%,136%;在异型增生的检出率各为857%,643%,286%;在早期胃癌的检出率各为167%,333%,111%;在进展期胃癌的检出率各为50%,525%,550%;在癌旁粘膜的Hp检出率为867%;在癌前病变中,Hp阳性组的p53,cerbB2表达率均高于Hp阴性组.结论Hp感染参与了胃癌前病变的发生与发展;Hp感染可引起野生型p53基因失活和cerbB2基因激活,从而导致胃粘膜的癌变. AIM To study the relationship between Helicobacter pylori infection and p53, c erbB 2 gene expression in carcinogenesis of gastric mucosa. METHODS Sixteen cases of superficial gastritis, 22 intestinal metaplasia, 14 dysplasia, 18 early gastric cancer and 40 advanced gastric cancer were studied. Hp was detected by Warthin Starry Ag staining, and p53, c erbB 2 gene expression were detected by Sp immunohistochemical method. RESULTS Hp, p53 and c erbB 2 positive rates were 50 0%, 0 0%, and 0 0% in superficial gastritis, 59 1%, 22 7% and 13 6% in intestinal metaplasia and 85 7%, 64 3% and 28 6% in dysplasia respectively. The positive rates were 16 7%, 33 3% and 11 1% in early gastric cancer and 5 0%, 52 5% and 55 0% in advanced gastric cancer. The positive rate of Hp in adjacent cancer mucosa was 86 7%. In precancerous lesions, the positive rates of p53 and c erbB 2 in Hp (+) group were higher than in Hp (-) group. CONCLUSION Hp infection plays a certain role in the pathogenesis of gastric precancerous lesions. Hp infection causes the inactivation of wild type p53 gene and activation of c erbB 2 gene, resulting in the occurrence of gastric cancer.
出处 《世界华人消化杂志》 CAS 1999年第4期313-315,共3页 World Chinese Journal of Digestology
关键词 胃肿瘤 幽门螺杆 P53基因 C-ERBB-2基因 stomach neoplasms Helicobacter pylori p53 gene c erbB 2 gene gene expression immunohistochemistry
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