Helicobacter pylori induced gastric carcinogenesis - The best molecular model we have?
Link A, Bornschein J, Thon C (2021)
Publication Type: Journal article, Review article
Publication year: 2021
Journal
Book Volume: 50-51
Article Number: 101743
DOI: 10.1016/j.bpg.2021.101743
Abstract
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.
Involved external institutions
Germany (DE)
United Kingdom (GB)How to cite
APA:
Link, A., Bornschein, J., & Thon, C. (2021). Helicobacter pylori induced gastric carcinogenesis - The best molecular model we have? Best Practice & Research in Clinical Gastroenterology, 50-51. https://doi.org/10.1016/j.bpg.2021.101743
MLA:
Link, Alexander, Jan Bornschein, and Cosima Thon. "Helicobacter pylori induced gastric carcinogenesis - The best molecular model we have?" Best Practice & Research in Clinical Gastroenterology 50-51 (2021).
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