Experiment Study On The Pathogenesis Of Gastric Carcinoma By Helicobacter Pylori And The Mechanism Of Chemoprevention

Objective: Researches in epidemiology, histopathology and animal experiment demonstrate that Helicobacter pylori (H. pylori ) is relevant to gastric carcinogenesis. Therefore, the World Health Organization International Agency for Research on Cancer confirms it is a carcinogen of gastric cacinoma. But the pathogenesis of gastric carcinogenesis in human remains unclear. Some studies indicate that H. pylori infection can up-regulate the expression of cyclooxygenase-2(COX-2) that induces gastric carcinogenesis by COX-2 dependent pathway and that their molecule mechanisms need further investigation. The carcinogenesis roles of cagA~+ H. pylori and cagA~- H. pylori in COX-2 dependent pathway are controversial. Studies show that the expression of COX-2 relates to dedifferentiation of human hepatocellular carcinoma. Whether the expression of COX-2 relates to dedifferentiation of gastric carcinoma is unclear. And up to now there are no report about the different role by H. pylori inducing in genesis and development in dedifferentiation of gastric carcinoma. Our experiment is to explore the molecule mechanisms of gastric carcinoma induced by H. pylori in human through COX-2 pathway and to study the role of cagA and the relationship between H. pylori and dedifferentiation of gastric carcinoma.One task of digestiology investigators and clinical workers is to study digestive neoplastic chemoprevention and to reduce morbidity and mortality by this way. Key steps or rate-limiting enzyme can act as the target of chemoprevention in tumorigenesis. Nonsteroid anti-inflammatory drugs (NSAIDs) or COX-2 inhibitor can reduce colon carcinogenesis in human and animals and can also reduce the number and size of polypous in familial polyposis coli according to epidemiological invesgations, animal experiments and clinical studies. Similar researches in gastric cancer are less. Some studies...