A20 (TNFAIP3) genetic alterations in EBV-associated AIDS-related lymphoma Academic Article uri icon

Overview

MeSH Major

  • Epstein-Barr Virus Infections
  • Intracellular Signaling Peptides and Proteins
  • Lymphoma, AIDS-Related
  • Mutation
  • Nuclear Proteins

abstract

  • A20, a negative regulator of NF-κB, has been implicated as a tumor suppressor gene in multiple types of B-cell lymphoma. AIDS-related lymphomas (ARLs) are high-grade B-cell lymphomas that are frequently associated with EBV infection. We examined a panel of ARLs for A20 alterations. FISH showed A20 deletion in 6 of 33 cases (18%). A20 mutations were found in 3 of 19 cases (16%), including 2 cases with deletions of the comple-mentary allele. Immunohistochemistry showed the absence of A20 protein in 7 of 55 samples (13%). In contrast to reports in Hodgkin lymphoma in which EBV infection and A20 alteration are mutually exclusive, A20 inactivation was observed in both EBV(+) and EBV(-) cases. The EBV latent membrane protein 1, which activates NF-κB, was not expressed in 12 of 13 cases with A20 loss. In ARLs loss of A20 may be an alternative mechanism of NF-κB activation in the absence of latent membrane protein 1 expression.

publication date

  • May 5, 2011

Research

keywords

  • Academic Article

Identity

Language

  • eng

PubMed Central ID

  • PMC3100694

Digital Object Identifier (DOI)

  • 10.1182/blood-2010-10-310995

PubMed ID

  • 21406721

Additional Document Info

start page

  • 4852

end page

  • 4

volume

  • 117

number

  • 18