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Enhancing Tumor Content through Tumor Macrodissection
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BCL2 mutations in diffuse large B-cell lymphoma.

J M Schuetz1, N A Johnson, R D Morin

  • 1Canada's Michael Smith Genome Sciences Center, BC Cancer Agency, University of British Columbia, Vancouver, British Columbia, Canada.

Leukemia
|December 23, 2011
PubMed
Summary
This summary is machine-generated.

BCL2 mutations are frequent in germinal center B-cell DLBCL and follicular lymphoma, often occurring alongside translocations. These mutations, however, do not independently impact survival in DLBCL.

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Immunoglobulin Gene Sequence Analysis In Chronic Lymphocytic Leukemia: From Patient Material To Sequence Interpretation
09:02

Immunoglobulin Gene Sequence Analysis In Chronic Lymphocytic Leukemia: From Patient Material To Sequence Interpretation

Published on: November 26, 2018

Area of Science:

  • Hematology
  • Oncology
  • Molecular Biology

Background:

  • BCL2 deregulation is a key event in diffuse large B-cell lymphoma (DLBCL), driven by translocations, amplification, or NF-κB signaling.
  • Recent RNA-seq data highlight BCL2 as the most mutated gene in germinal center B-cell (GCB) DLBCL.
  • Understanding BCL2 mutation patterns is crucial for diagnosing and treating B-cell lymphomas.

Purpose of the Study:

  • To comprehensively analyze BCL2 gene mutations across various non-Hodgkin lymphoma subtypes.
  • To investigate the correlation between BCL2 mutations, translocations, and clinical outcomes in DLBCL.
  • To determine the impact of BCL2 mutations on protein expression in DLBCL.

Main Methods:

  • Sequencing of the BCL2 gene in 298 primary DLBCL biopsies, 131 other non-Hodgkin lymphoma biopsies, 24 DLBCL cell lines, and 51 germline DNAs.
  • Analysis of mutation frequency, type, and location within the BCL2 gene.
  • Assessment of the relationship between BCL2 mutations, translocations, and patient survival.
  • Evaluation of BCL2 protein expression in relation to mutations.

Main Results:

  • Frequent BCL2 mutations were observed in follicular lymphoma (FL) and GCB DLBCL.
  • Low frequencies of BCL2 mutations were found in activated B-cell DLBCL, mantle cell lymphoma, small lymphocytic leukemia, and peripheral T-cell lymphoma.
  • No BCL2 mutations were detected in germinal center centroblasts.
  • Mutations were predominantly non-synonymous, located in the flexible loop domain, and consistent with somatic hypermutation.
  • BCL2 translocations correlated with additional BCL2 mutations in GCB DLBCL and FL.
  • BCL2 mutations were not independently associated with survival in DLBCL.
  • Pseudo-negative BCL2 protein expression due to mutations was rare in de novo DLBCL.

Conclusions:

  • BCL2 mutations are a common feature of GCB DLBCL and FL, often associated with translocations and somatic hypermutation.
  • The presence of BCL2 mutations does not appear to be an independent prognostic factor for survival in DLBCL.
  • While BCL2 mutations can occur, they rarely lead to pseudo-negative protein expression in de novo DLBCL, unlike in FL.