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Generation and characterization of the Eµ-Irf8 mouse model.

Zhijun Qiu1, Kenneth N Holder2, An-Ping Lin1

  • 1Division of Hematology and Medical Oncology, Department of Medicine, University of Texas Health Science Center San Antonio, San Antonio, TX 78229, USA.

Cancer Genetics
|June 15, 2020
PubMed
Summary

Chromosomal translocations in mature B-cell lymphomas can deregulate the IRF8 transcription factor. An Eµ-Irf8 mouse model showed altered B-cell development but no increased lymphoma incidence, suggesting a second genetic hit is needed.

Keywords:
Chromosomal translocationLymphomaTranscription factor

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Area of Science:

  • * Hematologic Oncology
  • * Molecular Biology
  • * Immunology

Background:

  • * Chromosomal translocations in mature B-cell malignancies frequently involve oncogenes juxtaposed to immunoglobulin regulatory regions.
  • * The t(14;16) translocation in diffuse large B-cell lymphoma (DLBCL) targets the transcription factor IRF8, which is also mutated in ~10% of DLBCLs.
  • * IRF8's role in myeloid/dendritic cells is known, but its specific contribution to mature B-cell malignancies remains unclear.

Purpose of the Study:

  • * To investigate the role of IRF8 deregulation in B-cell lymphomagenesis.
  • * To generate and characterize a mouse model (Eµ-Irf8) mimicking IRF8 deregulation seen in DLBCL.

Main Methods:

  • * Generation of the Eµ-Irf8 transgenic mouse model.
  • * Analysis of B-cell development and populations in bone marrow and spleen.
  • * Assessment of gene expression for known IRF8 targets (Aicda, Bcl6) in mature B-cells.
  • * Monitoring of lymphoma incidence and survival rates in Eµ-Irf8 mice compared to wild-type (WT) controls.

Main Results:

  • * Eµ-Irf8 mice exhibited normal development and peripheral blood parameters.
  • * Accumulation of pre-pro-B-cells and transitional B-cells was observed in Eµ-Irf8 mice.
  • * Overexpression of lymphomagenic IRF8 targets, Aicda and Bcl6, occurred in mature B-cells.
  • * No significant increase in B-cell lymphoma incidence was detected in Eµ-Irf8 mice, despite reduced survival.

Conclusions:

  • * IRF8 deregulation, as modeled in Eµ-Irf8 mice, impacts B-cell development but does not fully drive lymphomagenesis on its own.
  • * The observed phenotype suggests incomplete penetrance of IRF8's pro-lymphoma effects.
  • * A second genetic hit may be required to fully manifest the oncogenic potential of IRF8 in B-cell malignancies.