Hp Infection And Cox-2 Expression In Gastric Cancer And Precancerous Lesions

Gastric carcinoma ranks the first among all gastroenterol carcinomas worldwhile. Recent investigations have demonstrated carcinogenesis and development is a pathological process of multifactor , multistep and multigene alteration. In normal situation, the proliferation and apoptosis of gastric epithelial cell keep a balance , which is the base of structure and function. The balance is regulated by pro-oncogene, suppressor oncogene and some regulatory peptide. Though the pathogenesis of gastic carcinoma is unclear,multifactor may involve in the carcinogenesis and development of gastric carcinoma, for example, H. pylori, environment and heredity. The carcinogenic mechanism of H. pylori has been studied several years. Under the action of multicarcinogenic factors, pro-oncogenes are activated and suppressor oncogenes are inhibited, which makes the cell proliferation quickly, so the DNA damages increase. When the DNA damages are not repaired in time or do not induce apoptosis, the cell may develop into carcinoma cell. H. pylori, the main cause of chronic gastritis, has been defined as a class I gastric carcinogen. Gstric carcinogenesis is a multistep process progessing from gastritis though glandular atrophy, metaplysia and dysplasia. COX is a kind of membrane tuberculosis protein with the double functions of COX and synzyme. There are two kinds of COX: COX-1 and COX-2 . Some research works show that COX-2 is correlated with malignant tumor's growing, developing, metastases and differentiation . We investigate the carcinogenic mechanism of H. pylori by studying the expression of COX-2 in gastric epithelial cell.RUT is used to detected H. pylori in all samples. Immunohistochemical staining is used to detect the expression of COX-2 in tissue specimens.