Gastric cancer (GC) is a world health burden, ranging as the second cause of
cancer death worldwide. Etiologically, GC arises not only from the combined effects of environmental factors and susceptible genetic variants but also from the accumulation of genetic and epigenetic alterations. In the last years, molecular oncobiology studies brought to light a number of genes that are implicated in gastric
carcinogenesis. This review is intended to focus on the recently described basic aspects that play key roles in the process of gastric
carcinogenesis. Genetic variants of the genes
IL-10,
IL-17, MUC1, MUC6, DNMT3B, SMAD4, and SERPINE1 have been reported to modify the risk of developing GC. Several genes have been newly associated with gastric
carcinogenesis, both through oncogenic activation (GSK3β, CD133, DSC2,
P-Cadherin, CDH17, CD168, CD44,
metalloproteinases MMP7 and MMP11, and a subset of
miRNAs) and through tumor suppressor gene inactivation mechanisms (TFF1, PDX1, BCL2L10, XRCC, psiTPTE-HERV, HAI-2, GRIK2, and RUNX3). It also addressed the role of the inflammatory mediator
cyclooxygenase-2 (COX-2) in the process of gastric
carcinogenesis and its importance as a potential molecular target for
therapy.