Molecular Biological Studies on Cellular Proliferation and Apoptosis Induced by H. pylori

H.幽门螺杆菌间接通过萎缩性胃炎和肠上皮化生，直接通过病原体引起的细胞增殖和抗凋亡。本研究探讨了CagA在激活细胞内信号转导中的作用和H. pylori感染的分子生物学水平，并揭示了cagPAI和CagA在每种现象中的作用。幽门螺杆菌预防胃癌的临床研究日本最近开始根除幽门螺杆菌。然而，由于大约有5000万人对H。pylori在日本，从经济角度和并发症（如反流性食管炎加重）来看，不分青红皂白地根除可能不可行。如果我们能够区分胃癌的高危人群，那么预防胃癌可能会变得实用，这将有助于理解H诱导的细胞增殖和抗凋亡的机制。幽门。

Gastric carcinogenesis may be induced by H. pylori indirectly through atrophic gastritis and intestinal metaplasia and directly through cellular proliferation and anti-apoptosis caused by the pathogen. We investigated in this study (1) the role played by CagA in the activation of intracellular signal transduction and (2) the suppression of apoptosis by H. pylori on molecular biological levels and revealed the role of cagPAI and CagA in each phenomenon. Clinical studies on the prevention of stomach cancer by H. pylori eradication has recently been started in Japan. However, since there are about 50 million people positive for H. pylori in Japan, indiscriminate eradication may not be feasible from the economic viewpoint and also concerning complications such as exacerbation of regurgitation esophagitis. Prevention of stomach cancer may become practical if we can discriminate those who are at a high risk for stomach cancer, which will be facilitated by the understanding of mechanisms underlying cellular proliferation and anti-apoptosis induced by H. pylori.