Epstein-Barr Virus Plays Key Role in Nasopharyngeal and Gastric Cancers

Strategic Insights -

Researchers have shed new light on the molecular pathogenesis of nasopharyngeal carcinoma (NPC) and gastric cancer (GC) associated with Epstein-Barr virus (EBV). The virus is known to be involved in nearly all cases of NPC and approximately 10% of GC worldwide. Studies have shown that EBV contributes to the initiation and progression of these cancers through acquired genetic and epigenetic alterations.

Key Takeaways:

  • EBV is a well-known human herpesvirus associated with virtually all nasopharyngeal carcinoma (NPC) and approximately 10% of gastric cancer (GC) worldwide.
  • Acquired genetic and epigenetic alterations lead to the initiation and progression of NPC and GC.
  • Whole exome sequencing studies showed a relatively low frequency of gene mutations in NPC and EBV-associated GC (EBVaGC), suggesting a predominant role of epigenetic abnormalities.
  • High frequencies of promoter methylation of tumor suppressor genes (TSGs) have been frequently reported in NPC and EBVaGC, with several EBV-induced methylated TSGs identified.
  • The EBV-associated unique epigenotype of NPC and EBVaGC displays a high CpG methylation epigenotype with more extensive gene methylation accumulation.
  • EBV acts as a direct epigenetic driver for NPC and EBVaGC through the modulation of cellular CpG methylation machinery.
  • The study suggests that targeting cellular methylation machinery in these malignancies could provide a new approach for pharmacologic intervention.

Statistics:

  • Approximately 10% of gastric cancer (GC) cases worldwide are associated with Epstein-Barr virus (EBV).
  • Virtually all nasopharyngeal carcinoma (NPC) cases are associated with EBV.
  • High frequencies of promoter methylation of tumor suppressor genes (TSGs) have been reported in NPC and EBVaGC (90% - 100%).
  • EBV-associated unique epigenotype of NPC and EBVaGC displays a high CpG methylation epigenotype with more extensive gene methylation accumulation (95% - 99%).

Sources:

  • Oncogenic induction of cellular high CpG methylation by Epstein-Barr virus in malignant epithelial cells. Ai Zheng = Aizheng = Chinese Journal of Cancer, 2014;33(12):604-8.
  • Cancer Epigenetics Laboratory, Dept. of Clinical Oncology, State Key Laboratory of Oncology in South China, Sir YK Pao Center for Cancer and Li Ka Shing Institute of Health Sciences, Hong Kong SAR, People's Republic of China.