Molecular Pathogenesis of Gastric Cancer
Article first published online: 9 SEP 2013
© 2013 John Wiley & Sons Ltd
Special Issue: The Year in Helicobacter 2013. Guest Editors: Francis Mégraud and Peter Malfertheiner
Volume 18, Issue Supplement s1, pages 28–33, September 2013
How to Cite
Figueiredo, C., Garcia-Gonzalez, M. A. and Machado, J. C. (2013), Molecular Pathogenesis of Gastric Cancer. Helicobacter, 18: 28–33. doi: 10.1111/hel.12083
- Issue published online: 9 SEP 2013
- Article first published online: 9 SEP 2013
- Molecular pathology;
- DNA copy-number variations;
- tumor suppressor genes
Gastric carcinogenesis is a complex and multifactorial process, in which infection with Helicobacter pylori plays a major role. Additionally, environmental factors as well as genetic susceptibility factors are significant players in gastric cancer (GC) etiology.
Gastric cancer development results from the accumulation of multiple genetic and epigenetic changes during the lifetime of the cancer patient that will activate oncogenic and/or inactivate tumor-suppressor pathways. Numerous studies published last year provided new insights into the molecular phenotypes of GC, which will be the main focus of this review. This article also reviews the recent findings on GC tumor-suppressor genes, including putative novel genes.
The understanding of the basic mechanisms that underlie gastric carcinogenesis will be of utmost importance for developing strategies of screening, early detection, and treatment of the disease, as most GC patients present with late-stage disease and have poor overall survival.