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BCR and TLR signaling pathways are recurrently targeted by genetic changes in splenic marginal zone lymphomas

Qingguo Yan1, Yuanxue Huang, A James Watkins

  • 1Division of Molecular Histopathology, Department of Pathology, University of Cambridge, Cambridge, UK.

Haematologica
|November 22, 2011
PubMed

Insights

Genetic changes in NF-κB regulators like A20 and MYD88 are implicated in splenic marginal zone lymphoma pathogenesis. These mutations suggest the toll-like receptor and B-cell receptor pathways are key in this lymphoma.

Area of Science:

  • Hematology
  • Oncology
  • Molecular Biology

Background:

  • The genetic basis and development of splenic marginal zone lymphoma (SMZL) remain largely unclear.
  • While 7q deletion is observed in about 30% of SMZL cases, the specific gene affected is unknown.
  • Previous research indicated A20 inactivation in a small subset of SMZL, suggesting potential involvement of the NF-κB pathway.

Purpose of the Study:

  • To investigate the role of NF-κB pathway deregulation in the pathogenesis of splenic marginal zone lymphoma.
  • To screen key NF-κB regulators for genetic alterations in SMZL.

Main Methods:

  • Polymerase Chain Reaction (PCR) and DNA sequencing were employed to screen for somatic mutations.
  • Specific NF-κB regulators including A20, MYD88, CARD11, CD79A, CD79B, and ABIN1 were analyzed.

Main Results:

  • Somatic mutations were identified in A20 (13%), MYD88 (13%), and CARD11 (8.8%).
  • No mutations were found in CD79A, CD79B, or ABIN1.
  • The observed genetic alterations, particularly MYD88 mutations, were largely mutually exclusive with each other and with 7q deletion.

Conclusions:

  • Deregulation of the toll-like receptor (TLR) and B-cell receptor (BCR) signaling pathways is strongly suggested to be crucial in SMZL pathogenesis.
  • Mutations in A20, MYD88, and CARD11 point towards the involvement of these key signaling pathways in the development of splenic marginal zone lymphoma.

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