Published online Oct 14, 2014. doi: 10.3748/wjg.v20.i38.13804
Revised: April 30, 2014
Accepted: May 28, 2014
Published online: October 14, 2014
Gastric cancer (GC) is a major public health issue as the fourth most common cancer and the second leading cause of cancer-related death. Recent advances have improved our understanding of its molecular pathogenesis, as best exemplified by elucidating the fundamental role of several major signaling pathways and related molecular derangements. Central to these mechanisms are the genetic and epigenetic alterations in these signaling pathways, such as gene mutations, copy number variants, aberrant gene methylation and histone modification, nucleosome positioning, and microRNAs. Some of these genetic/epigenetic alterations represent effective diagnostic and prognostic biomarkers and therapeutic targets for GC. This information has now opened unprecedented opportunities for better understanding of the molecular mechanisms of gastric carcinogenesis and the development of novel therapeutic strategies for this cancer. The pathogenetic mechanisms of GC are the focus of this review.
Core tip: Gastric cancer (GC) is a complex, multistep process involving environmental factors and deregulation of canonical oncogenic pathways. Central to these mechanisms are the genetic and epigenetic alterations in these oncogenic signaling pathways. We discuss the recent remarkable progress in understanding the molecular mechanisms and the opening of unprecedented opportunities for the development of novel therapeutic strategies for GC.