The Role of EBV-Induced Hypermethylation in Gastric Cancer Tumorigenesis.

Journal Article (Journal Article;Review)

Epstein-Barr-virus-associated Gastric Cancer (EBVaGC) comprises approximately 10% of global gastric cancers and is known to be the most hypermethylated of all tumor types. EBV infection has been shown to directly induce the hypermethylation of both the host and viral genome following initial infection of gastric epithelial cells. Many studies have been completed in an attempt to identify genes that frequently become hypermethylated and therefore significant pathways that become silenced to promote tumorigenesis. It is clear that EBV-induced hypermethylation silences key tumor suppressor genes, cell cycle genes and cellular differentiation factors to promote a highly proliferative and poorly differentiated cell population. EBV infection has been shown to induce methylation in additional malignancies including Nasopharyngeal Carcinoma and Burkitt's Lymphoma though not to the same level as in EBVaGC. Lastly, some genes silenced in EBVaGC are common to other heavily methylated tumors such as colorectal and breast tumors; however, some genes are unique to EBVaGC and can provide insights into the major pathways involved in tumorigenesis.

Full Text

Duke Authors

Cited Authors

  • Stanland, LJ; Luftig, MA

Published Date

  • October 28, 2020

Published In

Volume / Issue

  • 12 / 11

PubMed ID

  • 33126718

Pubmed Central ID

  • PMC7693998

Electronic International Standard Serial Number (EISSN)

  • 1999-4915

Digital Object Identifier (DOI)

  • 10.3390/v12111222


  • eng

Conference Location

  • Switzerland