| [ Summary ] |
Gastric cancer may be classified into two groups, Helicobacter pylori (H. pylori)-related and unrelated. In regions, including Japan, where gastric cancer incidence is high, the great majority is of the former type. H. pylori-related gastric cancer progresses from infections, to gastric atrophy, and carcinogenesis. In each step, there seem to be specific environmental factors and genetic traits. Infection may be influenced by poor sanitary conditions and genetic polymorphisms associated with gastric acid secretion. Gastric atrophy may develop due to lifestyle on genotypes prone to inflammation, as well as polymorphisms responding to H. pylori pathogens. An association was found with a polymorphism of PTPN11 encoding SHP-2, which reacts with H. pylori CagA. Carcinogens and functional polymorphisms involved in carcinogenesis are thought to determine gastric cancer risk. Those with gastric atrophy are at high risk, to whom smoking cessation, high vegetable and fruit intakes, and lower dietary sodium intakes are recommended for reducing the risk. |