Cited by 183Lymphoma Diagnosis and TreatmentGenomics and Chromatin DynamicsT-cell and B-cell Immunology

Breaking bad in the germinal center: how deregulation of BCL6 contributes to lymphomagenesis

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Hatzi, Katerina, Melnick, Ari·2014·Trends in Molecular Medicine

Abstract

The B cell lymphoma 6 (BCL6) transcriptional repressor is a master regulator of the germinal center (GC) B cell program, required for their unique proliferative and stress tolerant phenotype. Most B cell lymphomas arise from GC B cells and are dependent on the continued or deregulated expression of BCL6 to maintain their survival. The actions of BCL6 in B cells involve formation of distinct chromatin modifying complexes that silence specific promoter and enhancer networks, respectively. The same biochemical mechanisms are maintained in malignant lymphoma cells. Targeted inhibition of these BCL6 functions has emerged as the basis for rational design of lymphoma therapies and combinatorial regimens. In this review, we summarize recent advances on BCL6 mechanisms of action and the deregulation of its target gene networks in lymphoma.

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Crossref · 10.1016/j.molmed.2014.03.001

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  • BCL6 is a non-enzymatic oncogenic driver of several B cell malignancies, including diffuse large B cell lymphoma (DLBCL) and follicular lymphoma.

    “Bcl6 is a non-enzymatic oncogenic driver of several B cell malignancies, diffuse large B cell lymphoma (DlBcl) and follicular lymphoma (Hatzi and Melnick 2014).”

    From From serendipity to strategy: molecular glue degraders in cancer therapeutics (2025) · cites this paper as Hatzi and Melnick 2014

  • Pathologically increased BCL6 expression, as a result of somatic BCL6 translocation, exonic mutation, promoter mutation, or mutations in regulatory pathways, is a common driver of B cell malignancies.

    “Pathologically increased BCL6 expression, as a result of somatic BCL6 translocation, exonic mutation, promoter mutation, or mutations in regulatory pathways, is a common driver of B cell malignancies16.”
  • BCL6 acts as a master transcriptional repressor enabling rapid expansion of germinal center B cells and tolerance to genomic instability caused by hypermutation of immunoglobulin genes and class switch recombination.

    “BCL6 acts as a master transcriptional repressor enabling rapid expansion of germinal center (GC) B cells and tolerance to genomic instability caused by hypermutation of the immunoglobulin genes and class switch recombination16.”

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Authors
Hatzi, K., & Melnick, A.
Affiliations
Weill Cornell Medicine (US)
Corresponding author
Melnick, Ari
Venue
Trends in Molecular Medicine
Publisher
Elsevier BV
Published
2014-06
Volume
20
Issue
6
Pages
343-352
ISSN
1471-4914 (ISSN-L)
OpenAlex
W1966652028
Cited by
183
References
76
Citations by year
2026: 7 · 2025: 19 · 2024: 8 · 2023: 14 · 2022: 17 · 2021: 19 · 2020: 18 · 2019: 16 · 2018: 19 · 2017: 12 · 2016: 12 · 2015: 16 · 2014: 6
FWCI
2.13
Type
journal article
Language
en
Open access
Locations
  • Trends in Molecular Medicine (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
National Cancer Institute (R01CA104348, R01CA143032)
Topics
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Lymphoma Diagnosis and Treatment
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
  • Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
Keywords
BCL6, germinal center B cells, B-cell lymphoma, lymphomagenesis, transcriptional repression, chromatin-modifying complexes, enhancer silencing, promoter silencing, BCL6 inhibitors, lymphoma treatment
MeSH terms
Cell Survival, DNA-Binding Proteins, Enhancer Elements, Genetic, Gene Expression Regulation, Humans, Immune System, Promoter Regions, Genetic, Gene Expression Regulation, Neoplastic, Lymphoma, B-Cell, Epigenesis, Genetic, Proto-Oncogene Proteins c-bcl-6, Molecular Targeted Therapy

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