Epstein-Barr virus in Burkitt's lymphoma: A role for latent membrane protein 2A

Kathryn T. Bieging, Michelle Swanson-Mungerson, Alexandra C. Amick, Richard Longnecker*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

31 Scopus citations


Burkitt's lymphoma (BL) is characterized by translocation of the MYC gene to an immunoglobulin locus. Transgenic mouse models have been used to study the molecular changes that are necessary to bypass tumor suppression in the presence of translocated MYC. Inactivation of the p53 pathway is a major step to tumor formation in mouse models that is also seen in human disease. Human BL is often highly associated with Epstein-Barr virus (EBV). The EBV latency protein latent membrane protein 2A (LMP2A) is known to promote B cell survival by affecting levels of pro-survival factors. Using LMP2A transgenic mouse models, we have identified a novel mechanism that permits lymphomagenesis in the presence of an intact p53 pathway. This work uncovers a contribution of EBV to molecular events that have documented importance in BL pathogenesis, and may underlie the poorly understood link between EBV and BL.

Original languageEnglish (US)
Pages (from-to)901-908
Number of pages8
JournalCell Cycle
Issue number5
StatePublished - Mar 1 2010


  • Apoptosis
  • Burkitt's lymphoma
  • Epstein-Barr virus
  • LMP2A
  • Myc
  • Viral oncogenesis
  • p53

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology
  • Developmental Biology


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