Peek Richard M, Crabtree Jean E
Division of Gastroenterology, Department of Medicine and Cancer Biology, Vanderbilt University School of Medicine, Nashville, TN 37232, USA.
J Pathol. 2006 Jan;208(2):233-48. doi: 10.1002/path.1868.
Chronic gastritis induced by Helicobacter pylori is the strongest known risk factor for adenocarcinoma of the distal stomach, yet only a minority of people who harbour this organism ever develop cancer. H. pylori isolates possess substantial genotypic diversity, which engenders differential host inflammatory responses that influence clinical outcome. H. pylori strains that possess the cag pathogenicity island and secrete a functional cytotoxin induce more severe gastric injury and further augment the risk for developing distal gastric cancer. However, carcinogenesis is also influenced by host genetic diversity, particularly involving immune response genes such as IL-1ss and TNF-alpha. It is important to gain insight into the pathogenesis of H. pylori-induced gastritis and adenocarcinoma, not only to develop more effective treatments for gastric cancer, but also because it might serve as a paradigm for the role of chronic inflammation in the genesis of other malignancies that arise within the gastrointestinal tract.
幽门螺杆菌引起的慢性胃炎是已知的远端胃癌最强风险因素，但携带这种微生物的人中只有少数会患癌。幽门螺杆菌菌株具有显著的基因型多样性，这会引发不同的宿主炎症反应，进而影响临床结果。拥有细胞毒素相关基因（cag）致病岛并分泌功能性细胞毒素的幽门螺杆菌菌株会导致更严重的胃损伤，并进一步增加患远端胃癌的风险。然而，致癌作用也受到宿主基因多样性的影响，特别是涉及白细胞介素-1β（IL-1β）和肿瘤坏死因子-α（TNF-α）等免疫反应基因。深入了解幽门螺杆菌引起的胃炎和腺癌的发病机制很重要，这不仅是为了开发更有效的胃癌治疗方法，还因为它可能成为慢性炎症在胃肠道内发生的其他恶性肿瘤发生过程中所起作用的范例。
