DNA hypermethylation induced by Epstein-Barr virus in the development of Epstein-Barr virus-associated gastric carcinoma

Research output: Contribution to journalReviewResearchpeer-review

  • Su Jin Choi
  • Yu Su Shin
  • Byung Woog Kang
  • Jong Gwang Kim
  • Won, Kyoung Jae
  • Paul M Lieberman
  • Hyosun Cho
  • Hyojeung Kang

Epstein-Barr virus (EBV)-associated gastric carcinoma (EBVaGC) is a recently recognized disease entity defined by the presence of EBV in gastric carcinoma cells. EBV infection causes major epigenetic alterations in the EBV genome and its cellular host genome, suggesting that EBV acts as a direct epigenetic driver for EBVaGC. One of the major epigenetic events in the viral and cellular genomes to control transcription is DNA hypo- or hyper-methylation. Particularly, local and global hypermethylation have been reported in EBVaGC. It is therefore important to understand the molecular mechanisms of DNA hypermethylation during EBVaGC carcinogenesis. To understand the functional roles of DNA methylation and suggest therapeutic target candidates for EBVaGC, we reviewed recent literature reporting DNA hypermethylation in EBVaGC. We summarized the identified candidate genes that are markedly hypermethylated in EBVaGC, which can potentially be targets for chemotherapies with demethylating agents.

Original languageEnglish
JournalArchives of Pharmacal Research
Issue number8
Pages (from-to)894-905
Number of pages12
Publication statusPublished - Aug 2017
Externally publishedYes

ID: 199325668