Gastric carcinogenesis can be described as a consequence of multilevel molecular alterations that is triggered by a cascade of events. Historically, diet and environmental factors have been identified to substantially contribute to carcinogenesis before the discovery of Helicobacter pylori (H. pylori). But H. pylori infection has revolutionized the understanding of gastric carcinogenesis. Although the model of H. pylori-driven carcinogenesis remains valid, there is a continuous effort to precisely delineate the molecular pathways involved and to understand the interplay with additional risk factors including recent relevant knowledge on the stomach microbiota. In this review, we provide an updated view on the models of gastric carcinogenesis. This includes historically appreciated H. pylori-induced models and expands these taking recent molecular data into consideration. Based on the data provided, we conclude that indeed H. pylori-carcinogenesis remains one of the best-established models at least for a subset of gastric cancers. Implementation of the recently identified molecular subtypes in novel genetic animal models is required to expand our knowledge on H. pylori-independent carcinogenesis.

胃癌的发生可以描述为由一系列事件触发的多水平分子改变的结果。历史上，在发现幽门螺杆菌（H. pylori）之前，已经确定饮食和环境因素对致癌作用起了重要作用。但是幽门螺杆菌感染已经彻底改变了对胃癌发生的认识。虽然幽门螺杆菌的模型驱动的致癌作用仍然有效，人们一直在努力精确地描述所涉及的分子途径，并了解与其他危险因素（包括有关胃微生物的最新相关知识）之间的相互作用。在这篇综述中，我们提供了关于胃癌发生模型的最新观点。这包括历史上公认的幽门螺杆菌诱导的模型，并考虑了最近的分子数据，对这些模型进行了扩展。根据提供的数据，我们得出结论，实际上幽门螺杆菌致癌作用至少在一部分胃癌中仍然是最完善的模型之一。扩大我们对幽门螺杆菌的认识需要在新型遗传动物模型中实施最近鉴定的分子亚型-独立的致癌作用。