ArticleNature genetics2022
SMARCE1 deficiency generates a targetable mSWI/SNF dependency in clear cell meningioma.
Article in Nature genetics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
31 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.
- European Association of Neuro-Oncology guideline on molecular testing of meningiomas for targeted therapy selection.Neuro-oncology · 2025Guideline
- Structural principles underlying the evolution of SWI/SNF chromatin remodelers.Science advances · 2026Article
- Epigenetic Alterations in Meningiomas-A Review.Biomedicines · 2026Review
- Chromatin Remodeller BRD9 Orchestrates Odontoblastic Differentiation via Coordinating RUNX2-KLF4.Cell proliferation · 2026Article
- The Wnt signaling networks in higher-grade meningiomas: from molecular pathogenesis to therapeutic innovation.Cancer cell international · 2026Review
- A comparative evaluation of canine meningioma supporting the canine patient as a naturally occurring animal model for human meningioma: a report from the NCI Comparative Brain Tumor Consortium (CBTC) meningioma pathology board.Veterinary oncology (London, England) · 2026Article
- Targeting SUMOylation promotes cBAF complex stabilization and disruption of the SS18::SSX transcriptome in synovial sarcoma.Nature communications · 2025Article
- Shifted assembly and function of mSWI/SNF family subcomplexes underlie targetable dependencies in dedifferentiated endometrial carcinomas.bioRxiv : the preprint server for biology · 2025Article
- Evolving Treatment Paradigms of Meningiomas; a Precision Medicine Perspective.Current neurology and neuroscience reports · 2025Review
- Nuclear glycine decarboxylase suppresses STAT1-dependent MHC-I and promotes cancer immune evasion.The EMBO journal · 2025Article
- Meningioma: Novel Diagnostic and Therapeutic Approaches.Biomedicines · 2025Review
- Predicting hepatocellular carcinoma outcomes and immune therapy response with ATP-dependent chromatin remodeling-related genes, highlighting MORF4L1 as a promising target.Cancer cell international · 2025Article
- Clear cell meningioma: Experience at a medical center.Surgical neurology international · 2025Article
- Smarce1 fine-tunes cardiomyocyte proliferation in the embryonic zebrafish heart.Frontiers in cell and developmental biology · 2025Article
- Meningioma: International Consortium on Meningiomas consensus review on scientific advances and treatment paradigms for clinicians, researchers, and patients.Neuro-oncology · 2024Review
- Chromatin remodellers as therapeutic targets.Nature reviews. Drug discovery · 2024Review
- Mammalian SWI/SNF complex activity regulates POU2F3 and constitutes a targetable dependency in small cell lung cancer.Cancer cell · 2024Article
- Review
- Update on Cancer Predisposition Syndromes and Surveillance Guidelines for Childhood Brain Tumors.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024Review
- Review
Corrections and comments
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Authors and funding
15 authors at 6 institutions in 3 countries.
Funding
Abstract
Mammalian SWI/SNF (mSWI/SNF) ATP-dependent chromatin remodeling complexes establish and maintain chromatin accessibility and gene expression, and are frequently perturbed in cancer. Clear cell meningioma (CCM), an aggressive tumor of the central nervous system, is uniformly driven by loss of SMARCE1, an integral subunit of the mSWI/SNF core. Here, we identify a structural role for SMARCE1 in selectively stabilizing the canonical BAF (cBAF) complex core-ATPase module interaction. In CCM, cBAF complexes fail to stabilize on chromatin, reducing enhancer accessibility, and residual core module components increase the formation of BRD9-containing non-canonical BAF (ncBAF) complexes. Combined attenuation of cBAF function and increased ncBAF complex activity generates the CCM-specific gene expression signature, which is distinct from that of NF2-mutated meningiomas. Importantly, SMARCE1-deficient cells exhibit heightened sensitivity to small-molecule inhibition of ncBAF complexes. These data inform the function of a previously elusive SWI/SNF subunit and suggest potential therapeutic approaches for intractable SMARCE1-deficient CCM tumors.
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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.