ArticleCancer cell2024
SMARCA4 is a haploinsufficient B cell lymphoma tumor suppressor that fine-tunes centrocyte cell fate decisions.
Article in Cancer cell, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
22 citing papers in PubMed, 27 citations in OpenAlex.
- The roles of chromatin remodeling and 3D genome organization in cancers: from mechanistic insights to emerging treatment options.Molecular cancer · 2026Review
- Establishment and characterization of TRI-LC21: a novel patient-derived cell line of SMARCA4-deficient undifferentiated thoracic tumor.Human cell · 2026Article
- BRG1-mediated suppression of ferroptosis underlies BTK inhibitor resistance.Nature communications · 2026Article
- Osimertinib Resistance in EGFR-Mutated Non-Small Cell Lung Cancer: Mechanisms and Therapeutic Strategies.MedComm · 2026Review
- Next-generation sequencing elucidates the distinct mutational landscape of SMARCA4-deficient lung cancer.Oncology letters · 2026Article
- SMARCA4 mutations drive metastatic progression and predict poor survival in breast cancer based on a real-world cohort study.Discover oncology · 2026Article
- Molecular Pathogenesis and Therapeutic Response of Diffuse Large B Cell Lymphoma Genetic Subtypes.Annual review of cancer biology · 2026Article
- Chromatin Regulatory Targets for Anticancer Therapeutics.Chemical reviews · 2025Review
- Novel Molecular Insights and Evolution of Less Toxic Therapeutic Strategies in Burkitt Lymphoma.Cancers · 2025Review
- USF1-induced RPS6KB2 activation influences aggressive phenotype in B-cell non-Hodgkin lymphoma.Human cell · 2025Article
- SMARCA4 Inhibits Breast Cancer Progression and Metastasis through RHOA Suppression.Cancer research · 2025Article
- Audit of B-cell cancer genes.Blood advances · 2025Review
- MYC networks associate with decreased CD8 T-cell presence in diffuse large B-cell lymphoma and may be addressed by the synergistic combination of AZD4573 and Selinexor - a preliminary analysis.Annals of hematology · 2025Article
- Chromatin remodeling in lymphocytic function and fate: the multifaceted roles of SWI/SNF complex.Frontiers in immunology · 2025Review
- Bromodomain proteins as potential therapeutic targets for B-cell non-Hodgkin lymphoma.Cell & bioscience · 2024Review
- SMARCA5-mediated chromatin remodeling is required for germinal center formation.The Journal of experimental medicine · 2024Article
- Expanding the clinicopathologic spectrum and genomic landscape of tumors with SMARCA2/4::CREM fusions.The Journal of pathology · 2024Article
- Lack of SMARCB1 expression characterizes a subset of human and murine peripheral T-cell lymphomas.Nature communications · 2024Article
- Arid1a-dependent canonical BAF complex suppresses inflammatory programs to drive efficient germinal center B cell responses.Nature immunology · 2024Article
- Article
Corrections and comments
- Commented on by
Authors and funding
29 authors at 4 institutions in 1 country.
Funding
Abstract
SMARCA4 encodes one of two mutually exclusive ATPase subunits in the BRG/BRM associated factor (BAF) complex that is recruited by transcription factors (TFs) to drive chromatin accessibility and transcriptional activation. SMARCA4 is among the most recurrently mutated genes in human cancer, including ∼30% of germinal center (GC)-derived Burkitt lymphomas. In mice, GC-specific Smarca4 haploinsufficiency cooperated with MYC over-expression to drive lymphomagenesis. Furthermore, monoallelic Smarca4 deletion drove GC hyperplasia with centroblast polarization via significantly increased rates of centrocyte recycling to the dark zone. Mechanistically, Smarca4 loss reduced the activity of TFs that are activated in centrocytes to drive GC-exit, including SPI1 (PU.1), IRF family, and NF-κB. Loss of activity for these factors phenocopied aberrant BCL6 activity within murine centrocytes and human Burkitt lymphoma cells. SMARCA4 therefore facilitates chromatin accessibility for TFs that shape centrocyte trajectories, and loss of fine-control of these programs biases toward centroblast cell-fate, GC hyperplasia and lymphoma.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.