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

Study on Helicobacter pylori infection and p53 , c erbB 2 gene expression in carcinogenesis of gastric mucosa

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.