ArticleLeukemia2020
Frequent mutations in the amino-terminal domain of BCL7A impair its tumor suppressor role in DLBCL.
Article in Leukemia, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 46 citations in OpenAlex.
- Genetic and clinical insights into the coexistence of multiple myeloma and diffuse large B cell lymphoma from a case report and systematic review with bioinformatics analysis.Discover oncology · 2026Article
- Structure and molecular function of the BCL7 proteins.Biochemical Society transactions · 2026Review
- Article
- BCL7A's arginine anchor links nucleosome recognition to chromatin remodeling and diffuse large B-cell lymphoma tumor suppression.Protein & cell · 2026Article
- Loss of BCL7A permits IRF4 transcriptional activity and cellular growth in multiple myeloma.Blood · 2025Article
- Audit of B-cell cancer genes.Blood advances · 2025Review
- Structure of the nucleosome-bound human BCL7A.Nucleic acids research · 2025Article
- Epigenetic Symphony in Diffuse Large B-Cell Lymphoma: Orchestrating the Tumor Microenvironment.Biomedicines · 2025Review
- Identifying reproducible transcription regulator coexpression patterns with single cell transcriptomics.PLoS computational biology · 2025Article
- Single-cell RNA sequencing defines distinct disease subtypes and reveals hypo-responsiveness to interferon in asymptomatic Waldenstrom's Macroglobulinemia.Nature communications · 2025Article
- Plant BCL-DOMAIN HOMOLOG proteins play a conserved role in SWI/SNF complex stability.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Characterization of Freshly Isolated Human Peripheral Blood B Cells, Monocytes, CD4+ and CD8+ T Cells, and Skin Mast Cells by Quantitative Transcriptomics.International journal of molecular sciences · 2024Article
- Advances in epigenetic therapies for B-cell non-hodgkin lymphoma.Annals of hematology · 2024Review
- Prevention and treatment of peri-implant fibrosis by functionally inhibiting skeletal cells expressing the leptin receptor.Nature biomedical engineering · 2024Article
- Opening and changing: mammalian SWI/SNF complexes in organ development and carcinogenesis.Open biology · 2024Review
- Plant BCL-Domain Homologues play a conserved role in SWI/SNF complex stability.bioRxiv : the preprint server for biology · 2024Article
- Article
- Activation-induced cytidine deaminase causes recurrent splicing mutations in diffuse large B-cell lymphoma.Molecular cancer · 2024Article
- BCL7A and BCL7B potentiate SWI/SNF-complex-mediated chromatin accessibility to regulate gene expression and vegetative phase transition in plants.Nature communications · 2024Article
- BRG1 HSA domain interactions with BCL7 proteins are critical for remodeling and gene expression.Life science alliance · 2023Article
Corrections and comments
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Authors and funding
14 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations in genes encoding subunits of the SWI/SNF chromatin remodeling complex are frequently found in different human cancers. While the tumor suppressor function of this complex is widely established in solid tumors, its role in hematologic malignancies is largely unknown. Recurrent point mutations in BCL7A gene, encoding a subunit of the SWI/SNF complex, have been reported in diffuse large B-cell lymphoma (DLBCL), but their functional impact remains to be elucidated. Here we show that BCL7A often undergoes biallelic inactivation, including a previously unnoticed mutational hotspot in the splice donor site of intron one. The splice site mutations render a truncated BCL7A protein, lacking a portion of the amino-terminal domain. Moreover, restoration of wild-type BCL7A expression elicits a tumor suppressor-like phenotype in vitro and in vivo. In contrast, splice site mutations block the tumor suppressor function of BCL7A by preventing its binding to the SWI/SNF complex. We also show that BCL7A restoration induces transcriptomic changes in genes involved in B-cell activation. In addition, we report that SWI/SNF complex subunits harbor mutations in more than half of patients with germinal center B-cell (GCB)-DLBCL. Overall, this work demonstrates the tumor suppressor function of BCL7A in DLBCL, and highlights that the SWI/SNF complex plays a relevant role in DLBCL pathogenesis.
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