ArticleNature genetics2017
SMARCB1-mediated SWI/SNF complex function is essential for enhancer regulation.
Article in Nature genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 237 papers.
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Who cites it
237 citing papers in PubMed, 357 citations in OpenAlex.
- Tuning epigenetics to enhance cancer virotherapy.Acta pharmaceutica Sinica. B · 2026Review
- The roles of chromatin remodeling and 3D genome organization in cancers: from mechanistic insights to emerging treatment options.Molecular cancer · 2026Review
- Functional profiling of ovarian cancer models reveals Bcl-xL/NOTCH targeting to overcome resistance.NPJ precision oncology · 2026Article
- Loss-of-Function Mutations in SWI/SNF Complexes Associated With Active Tumour Immune Microenvironment Clinical Response to Immune Checkpoint Blockade.Journal of cellular and molecular medicine · 2026Article
- PBRM1-dependent PBAF targeting is required for EMT and metastasis in breast cancer.Science advances · 2026Article
- Relapsed rhabdoid tumours and other non-nephroblastoma childhood and adolescent kidney tumours: perspectives from the HARMONICA collaboration.Nature reviews. Urology · 2026Review
- Context-dependent synthetic lethality - an emerging precision therapeutic approach.Nature reviews. Cancer · 2026Review
- SMARCD1 and Its Functional Relevance in SWI/SNF and Cancer.International journal of molecular sciences · 2026Review
- ISWI remodeler facilitates cBAF genomic binding to drive cell fate transition.bioRxiv : the preprint server for biology · 2026Article
- SMARCA4 mutations drive metastatic progression and predict poor survival in breast cancer based on a real-world cohort study.Discover oncology · 2026Article
- BCL7A's arginine anchor links nucleosome recognition to chromatin remodeling and diffuse large B-cell lymphoma tumor suppression.Protein & cell · 2026Article
- SMARCB1 missense mutants disrupt SWI/SNF complex stability and remodeling activity.Nature communications · 2026Article
- PHIP suppresses NuRD to enable the growth of SWI/SNF-mutant cancers.Nature communications · 2026Article
- A SWI/SNF-specific Ig-like domain, SWIFT, is a transcription factor binding platform.Science (New York, N.Y.) · 2026Article
- Implications for clinical prognosis and target discovery of the SWI/SNF complex in genitourinary tumors.Discover oncology · 2026Review
- Canonical BAF chromatin remodeling complex specifies stem cell fate via cell-type-specific co-factor recruitment.Nature communications · 2026Article
- Schwannomatosis tumor modeling: progress and prospects for translational research.Journal of biological engineering · 2026Review
- SWI/SNF Chromatin Remodelling Complex in Hepatic Physiology: Mechanistic Insights Into Development, Homeostasis and Pathogenesis.Journal of cellular and molecular medicine · 2026Review
- Decoding UTROSCT heterogeneity: systematic clinicopathological evaluation combined with molecular profiling.The journal of pathology. Clinical research · 2026Article
- Disordered DNA methylation leads to targetable transcriptional plasticity in ATRT.Acta neuropathologica communications · 2025Article
177 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
18 authors at 6 institutions in 1 country.
Funding
Abstract
SMARCB1 (also known as SNF5, INI1, and BAF47), a core subunit of the SWI/SNF (BAF) chromatin-remodeling complex, is inactivated in nearly all pediatric rhabdoid tumors. These aggressive cancers are among the most genomically stable, suggesting an epigenetic mechanism by which SMARCB1 loss drives transformation. Here we show that, despite having indistinguishable mutational landscapes, human rhabdoid tumors exhibit distinct enhancer H3K27ac signatures, which identify remnants of differentiation programs. We show that SMARCB1 is required for the integrity of SWI/SNF complexes and that its loss alters enhancer targeting-markedly impairing SWI/SNF binding to typical enhancers, particularly those required for differentiation, while maintaining SWI/SNF binding at super-enhancers. We show that these retained super-enhancers are essential for rhabdoid tumor survival, including some that are shared by all subtypes, such as SPRY1, and other lineage-specific super-enhancers, such as SOX2 in brain-derived rhabdoid tumors. Taken together, our findings identify a new chromatin-based epigenetic mechanism underlying the tumor-suppressive activity of SMARCB1.
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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.