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

幽门螺杆菌可能通过萎缩性胃炎和肠化生间接诱导胃癌的发生，也可能直接通过病原体引起的细胞增殖和抗细胞凋亡而诱导胃癌的发生。本研究从分子生物学水平探讨了CagA在激活细胞内信号转导和抑制细胞凋亡中的作用，揭示了CagPAI和CagA在这两种现象中的作用。通过根除幽门螺杆菌预防胃癌的临床研究最近在日本开始。然而，由于日本约有5000万人幽门螺杆菌阳性，从经济学角度以及反流性食管炎加重等并发症的角度来看，无差别根除可能是不可行的。如果我们能够区分那些胃癌的高危人群，那么预防胃癌就有可能成为现实，这将有助于理解幽门螺杆菌诱导的细胞增殖和抗凋亡的机制。

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.