Causal role of Helicobacter pylori infection and eradication therapy in gastric carcinogenesis  

作　　者：Masanori Ito Shinji Tanaka Tomoari Kamada Ken Haruma Kazuaki Chayama 

机构地区：[1]Department of Medicine and Molecular Science,Hiroshima University,Hiroshima,Japan [2]Department of Endoscopy,Hiroshima University Hospital,Hiroshima,Japan [3]Gastroenterology Unit,Department of Internal Medicine,Kawasaki Medical School,Kurashiki,Japan

出　　处：《World Journal of Gastroenterology》2006年第1期10-16,共7页世界胃肠病学杂志（英文版）

摘　　要：Many epidemiological reports indicate that Helicobacter pylori （H pylori） infection plays an important role in gastric carcinogenesis. Several genetic and epigenetic alterations contribute to the initiation, promotion, and progression of the cancer cells in a multi-step manner. H pylori is known to induce chronic inflammation in the gastric mucosa. Its products, including superoxides, participate in the DNA damage followed by initiation, and the inflammation-derived cytokines and growth factors contribute to the promotion of gastric carcinogenesis. By eradicating H pylori, gastric inflammation can be cured; the therapy diminishes the levels not only of inflammatory cell infiltration, but also atrophy/ intestinal metaplasia in part. A randomized controlled trial revealed that the eradication therapy diminished the gastric cancer prevalence in cases without precancerous conditions. In addition, recent epidemiological studies from Japanese groups demonstrated that the development of gastric cancer, especially of the intestinal type, was decreased by successful eradication therapy, although these were designed in a non- randomized manner. However, it should be mentioned that endoscopic detection is the only way to evaluate the degree of gastric carcinogenesis. We have reported that the endoscopic and histological morphologies could be modified by eradication therapy and it might contribute to the prevalence of gastric cancer development. Considering the biological nature of cancer cell proliferation, it is considered that a sufficiently long-term follow-up would be essential to discuss the anticancer effect of eradication therapy.许多流行病学的报告显示感染玩的那 Helicobacter pylori (H pylori ) 在胃的致癌作用的一个重要角色。几基因、渐成说的改变以一种多步方式贡献癌症房间的开始，提升，和前进。H pylori 被知道在胃粘膜导致慢性炎。包括超级氧化物，它的产品参予开始跟随的 DNA 损坏，并且导出发炎的 cytokines 和生长因素贡献胃的致癌作用的提升。由根除 H pylori，胃的发炎能被治好；治疗减少不仅煽动性的房间渗入，而且 atrophy/intestinal 组织变形的层次部分地。使随机化的控制试用表明根除治疗减少了在没有癌症前期的条件的情况中的胃的癌症流行。另外，从日本组的最近的流行病学的研究证明特别肠的类型，胃的癌症的发展被成功的根除治疗减少，尽管这些以一种非使随机化的方式被设计。然而，内视镜的察觉是评估胃的致癌作用的度的唯一的方法，这应该被提及。我们报导了内视镜、组织学的形态学能被根除治疗修改，它可能贡献胃的癌症开发的流行。就癌症房间增长的生物性质而言，足够地长期的后续将是必要的讨论根除治疗的反癌症效果，这被考虑。

关 键 词：H pylori ERADICATION GASTRITIS Gastric neoplasm  Endoscopy 

分 类 号：R735.2[医药卫生—肿瘤]