H. pylori infection has a close relationship with the occurrence of gastric cancer, which can be demonstrated mainly from the following aspects: a. H. pylori infection is a key factor leading to the occurrence of gastric cancer H. pylori is considered to be the initiating and promoting factor of gastric cancer, which is an important etiology and promoting factor of precancerous lesions atrophic gastritis and intestinal epithelial metaplasia. In the International Agency for Research on Cancer (IARC), H. pylori is positioned as a class of oncogenic factors, and H. pylori infection is significantly associated with both the occurrence and progression of gastric cancer. H. pylori infection causes a large number of inflammatory cells to produce and release a variety of reactive oxygen compounds, causing cellular DNA mutations, chromosomal damage, and abnormal proliferation of mucosal cells, which leads to cancer. Patients with H. pylori infection have increased NO synthase activity in the gastric mucosa and greatly increased NO content, which has a toxic effect on mucosal cells and leads to mutation of cells into cancer cells. H. pylori also causes mutation of normal genes. H. pylori infection leads to activation of oncogenes, inactivation and mutation of oncogenes and damage to repair genes. Studies have shown that overexpression or mutation of the p53 gene and ras gene manifests as damage to the epithelial cells of the stomach and mutation of too many normal genes leads to tumorigenesis. Second, the epidemiology of H. pylori and gastric cancer is consistent with Most data show that the incidence of gastric cancer is directly proportional to the rate of H. pylori infection, especially the rate of H. pylori infection in areas with high incidence of gastric cancer is higher. The mortality rate of gastric cancer is positively correlated with the rate of H. pylori infection. It can be seen that there is a significant correlation between H. pylori infection and the incidence of gastric cancer. Third, H. pylori is highly correlated with the incidence of gastric cancer Studies have shown that more than 90% of duodenal ulcers and about 80% of gastric ulcers are caused by H. pylori infection, which causes mild chronic inflammation of the gastric mucosa or leads to gastric and duodenal ulcers and gastric cancer. Studies in areas with a high incidence of gastric cancer show that the prevalence of H. pylori infection in childhood is significantly higher than in areas with a low incidence of gastric cancer. People infected with H. pylori at a young age survive for a long time after infection and are more likely to develop chronic active gastritis and intestinal metaplasia, which increases the likelihood of gastric cancer. Fourth, the high correlation between H. pylori infection and precancerous lesions In recent years, precancerous lesions are highly valued by doctors and patients, and a large number of studies have confirmed that H. pylori infection is closely related to the occurrence of precancerous lesions of gastric cancer. The process from chronic gastritis to atrophic gastritis, then to intestinal chemosis, then to heterogeneous hyperplasia, and finally to gastric cancer usually takes more than ten years or even decades. Among them, H. pylori-positive people are more likely to develop atrophic gastritis than H. pylori-negative people, while intestinal chemosis in H. pylori-infected people is more inclined to develop toxic intestinal chemosis and incomplete intestinal chemosis, while atrophic gastritis and intestinal epithelial chemosis are one of the links in the process of gastric carcinogenesis. All of the above aspects indicate a close relationship between H. pylori and the occurrence of gastric cancer, and there are several theories about the mechanisms by which H. pylori infection causes gastric cancer: H. pylori causes accelerated proliferation of gastric mucosal epithelial cells; H. pylori causes increased apoptosis of gastric mucosal epithelial cells; abnormal genes and expression; H. pylori promotes the formation of oncogenic metabolites; H. pylori infection-induced immune The immune response induced by H. pylori infection is associated with the development of gastric cancer. Therefore, H. pylori eradication can help prevent gastric cancer, and most studies have shown that H. pylori eradication is an important means of preventing gastric cancer. However, definitive evidence for H. pylori eradication to prevent gastric cancer is lacking, so standardized eradication is currently preferred for those with precancerous lesions and family history of gastric cancer, and for those with early gastric tumor resection.