Skip to main content
. Author manuscript; available in PMC: 2019 May 1.
Published in final edited form as: Cancer Treat Rev. 2018 Mar 31;66:15–22. doi: 10.1016/j.ctrv.2018.03.006

Figure 1. Pathogenesis of EBVaGC.

Figure 1

Although the pathogenesis of EBVaGC is not clearly established, several factors allow EBV to stimulate oncogenesis in the gastric epithelium. Once EBV infects the gastric epithelial cell, it enters its latency phase and leads to genome-wide methylation and cell pathway regulation. Aberrant genetic expression and the interaction of EBV infected gastric epithelial cell with the tumor microenvironment dictates cell fate, ultimately leading to cancer development and epithelial to mesenchymal transition.