摘要
Gastric cancer remains a global killer with a shifting burden from the developed to the developing world. The cancer develops along a multistage process that is defined by distinct histological and pathophysiological phases. Several genetic and epigenetic alterations mediate the transition from one stage to another and these include mutations in oncogenes, tumour suppressor genes and cell cycle and mismatch repair genes. The most significant advance in the fight against gastric caner came with the recognition of the role of Helicobacter pylori （H pylori） as the most important acquired aetiological agent for this cancer. Recent work has focussed on elucidating the complex host/microbial interactions that underlie the neoplastic process. There is now considerable insight into the pathogenesis of this cancer and the prospect of preventing and eradicating the disease has become a reality. Perhaps more importantly, the study of H pylori-induced gastric carcinogenesis offers a paradigm for understanding more complex human cancers. In this review, we examine the molecular and cellular events that underlie Hpyloriinduced gastric cancer.
胃的癌症与变的负担仍然是一个全球杀手从发展了到发展中的世界。癌症沿着被定义由的一个多级式的过程发展不同组织学并且 pathophysiological 阶段。几基因、渐成说的改变调停从一个的转变上演到另外一个，这些在 oncogenes 包括变化，瘤压制或基因和房间骑车并且错配修理基因。在对胃的癌症的战斗的最重要的进展为这癌症作为最重要的获得的病因论的代理人与 Helicobacter pylori (H pylori ) 的角色的识别来了。最近的工作在阐明上集中了位于肿瘤的过程下面的复杂 host/microbial 相互作用。现在进这癌症的致病和阻止并且根除的前景有可观的卓见疾病成为了现实。也许更重要地， H 导致 pylori 的胃的致癌作用的学习为理解更复杂的人的癌症提供一个范例。在这评论，我们检验位于 H 下面的分子、细胞的事件导致 pylori 的胃的癌症。
