Clinicopathologic implication of A20/TNFAIP3 deletion in diffuse large B-cell lymphoma: an analysis according to immunohistochemical subgroups and rituximab treatment

Leuk Lymphoma. 2013 Sep;54(9):1934-41. doi: 10.3109/10428194.2012.762511. Epub 2013 Feb 16.

Abstract

We analyzed the clinicopathologic implication of A20/tumor necrosis factor α-induced protein 3 deletion in diffuse large B-cell lymphoma (DLBCL) using fluorescence in situ hybridization, according to germinal center B-cell (GCB) versus non-GCB/activated B-cell (ABC) phenotypes and rituximab treatment. Excluding primary central nervous system (CNS) and Epstein-Barr virus (EBV)-positive lymphomas, 134 DLBCLs were analyzed. A20 was deleted in 23.1% (31/134) of DLBCLs including 21.6% (29/ 134) of monoallelic and 1.5% (2/134) of biallelic deletion, with no predilection for GCB versus non-GCB/ABC. In univariate analysis, A20 deletion was marginally associated with favorable prognosis in the rituximab-treated subgroup (n = 109; p = 0.0454), non-gastrointestinal lymphoma (n = 108; p = 0.0320) and nodal lymphoma (n = 46; p = 0.0411). In multivariate analysis in rituximab-treated DLBCL, MUM1 and international prognostic index (IPI) were independent prognostic factors (p = 0.021 [IPI]; p = 009 [MUM1]) with a marginally favorable prognostic effect for A20 deletion (p = 0.047). Taken together, A20 deletion was observed in similar frequencies in GCB and non-GCB/ABC, and was not a poor prognostic factor in DLBCL.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Algorithms
  • Antibodies, Monoclonal, Murine-Derived / therapeutic use
  • Antineoplastic Agents / therapeutic use
  • DNA-Binding Proteins / genetics*
  • DNA-Binding Proteins / metabolism
  • Gene Deletion*
  • Humans
  • Immunohistochemistry
  • In Situ Hybridization, Fluorescence
  • Intracellular Signaling Peptides and Proteins / genetics*
  • Intracellular Signaling Peptides and Proteins / metabolism
  • Lymphoma, Large B-Cell, Diffuse / diagnosis*
  • Lymphoma, Large B-Cell, Diffuse / drug therapy
  • Lymphoma, Large B-Cell, Diffuse / genetics*
  • Lymphoma, Large B-Cell, Diffuse / mortality
  • Neoplasm Staging
  • Nuclear Proteins / genetics*
  • Nuclear Proteins / metabolism
  • Phenotype
  • Retrospective Studies
  • Rituximab
  • Tumor Necrosis Factor alpha-Induced Protein 3

Substances

  • Antibodies, Monoclonal, Murine-Derived
  • Antineoplastic Agents
  • DNA-Binding Proteins
  • Intracellular Signaling Peptides and Proteins
  • Nuclear Proteins
  • Rituximab
  • TNFAIP3 protein, human
  • Tumor Necrosis Factor alpha-Induced Protein 3