• Molecular pathology;
  • DNA copy-number variations;
  • mutations;
  • epigenetics;
  • 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.