A20 Mutation Is Not a Prognostic Marker for Activated B-Cell-Like Diffuse Large B-Cell Lymphoma

PLoS One. 2015 Dec 30;10(12):e0145037. doi: 10.1371/journal.pone.0145037. eCollection 2015.

Abstract

Background: Constitutive activation of nuclear factor κB (NF-κB) is a hallmark of activated B-cell-like diffuse large B-cell lymphoma (ABC-DLBCL). Mutations in the A20 gene activate NF-κB, but the prognostic value of A20 mutations in ABC-DLBLC is unclear.

Purpose: To investigate the prognostic value of A20 mutation in ABC-DLBCL patients.

Methods: The somatic mutation of A20 was investigated in 68 de novo ABC-DLBCLs by PCR/sequencing. The Kaplan-Meier method was used to estimate median overall survival (OS) and progression-free survival (PFS).

Results: The A20 mutation rate in ABC-DLBCL patients was 29.4%. Complete remission rates were 35% and 45.8% in patients with and without A20 mutations, respectively (P = 0.410). In patients with and without A20 mutations, the median OS was 24.0 and 30.6 months, respectively (P = 0.58), and the median PFS was 15 and 17.4 months, respectively (P = 0.52). None of the differences between the patient groups were significant.

Conclusions: Our findings suggested that the A20 mutation is a frequent event in ABC-DLBCLs. However, there was no significant difference in PFS and OS in patients with or without A20 mutations. Further study is required to completely exclude A20 somatic mutation as a prognostic marker in the ABC subtype of DLBLC.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • B-Lymphocytes / pathology*
  • Cell Survival / genetics
  • DNA-Binding Proteins / genetics*
  • Disease-Free Survival
  • Female
  • Humans
  • Intracellular Signaling Peptides and Proteins / genetics*
  • Lymphocyte Activation / genetics
  • Lymphoma, Large B-Cell, Diffuse / genetics*
  • Lymphoma, Large B-Cell, Diffuse / pathology*
  • Male
  • Middle Aged
  • Mutation / genetics*
  • NF-kappa B / genetics
  • Nuclear Proteins / genetics*
  • Prognosis
  • Signal Transduction / genetics
  • Tumor Necrosis Factor alpha-Induced Protein 3

Substances

  • DNA-Binding Proteins
  • Intracellular Signaling Peptides and Proteins
  • NF-kappa B
  • Nuclear Proteins
  • TNFAIP3 protein, human
  • Tumor Necrosis Factor alpha-Induced Protein 3

Grants and funding

This work was supported by the National Natural Science Foundation of China (81160298) and Key Grant of Health Department of Guangxi Province (2011077). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.