Evidence map›Paper›PMID 31015438›Full record

ArticleNature communications2019

BRD9 defines a SWI/SNF sub-complex and constitutes a specific vulnerability in malignant rhabdoid tumors.

Xiaofeng Wang, Su Wang, Emma C Troisi, Thomas P Howard, Jeffrey R Haswell, Bennett K Wolf, William H Hawk, Pilar Ramos, Elaine M Oberlick, Evgeni P Tzvetkov and 5 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 140 papers.

0numbers the graph read from it
0cells of the map it votes in
140citing papers in PubMed
8.1field-weighted citation impact, top 2% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

140 citing papers in PubMed, 212 citations in OpenAlex.

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  17. BRD9 at the crossroads of splicing, chromatin remodeling, and hematopoiesis.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2026
    Review
  18. Article
  19. Defective Microhomology-Mediated End-joining in SMARCB1-Deficient Tumors.bioRxiv : the preprint server for biology · 2025
    Article
  20. Article

80 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors at 5 institutions in 1 country.

Xiaofeng WangDepartment of Molecular and Systems Biology, Geisel School of Medicine, Dartmouth College, Hanover, NH, 03756, USA.
Su WangDepartment of Biomedical Informatics, Harvard Medical School, Boston, MA, 02115, USA.ORCID http://orcid.org/0000-0002-9463-6530
Emma C TroisiDepartment of Pediatric Oncology, Dana-Farber Cancer Institute, Boston, MA, 02215, USA.
Thomas P HowardDepartment of Pediatric Oncology, Dana-Farber Cancer Institute, Boston, MA, 02215, USA.ORCID http://orcid.org/0000-0002-3438-2831
Jeffrey R HaswellDepartment of Pediatric Oncology, Dana-Farber Cancer Institute, Boston, MA, 02215, USA.
Bennett K WolfDepartment of Molecular and Systems Biology, Geisel School of Medicine, Dartmouth College, Hanover, NH, 03756, USA.
William H HawkDepartment of Molecular and Systems Biology, Geisel School of Medicine, Dartmouth College, Hanover, NH, 03756, USA.
Pilar RamosComprehensive Cancer Center and Department of Oncology, St. Jude Children's Research Hospital, Memphis, TN, 38105, USA.
Elaine M OberlickDepartment of Pediatric Oncology, Dana-Farber Cancer Institute, Boston, MA, 02215, USA.
Evgeni P TzvetkovDepartment of Pediatric Oncology, Dana-Farber Cancer Institute, Boston, MA, 02215, USA.
Aaron RossComprehensive Cancer Center and Department of Oncology, St. Jude Children's Research Hospital, Memphis, TN, 38105, USA.
Francisca VazquezBroad Institute of Harvard and MIT, 415 Main Street, Cambridge, MA, 02142, USA.ORCID http://orcid.org/0000-0002-2857-4685
William C HahnBroad Institute of Harvard and MIT, 415 Main Street, Cambridge, MA, 02142, USA.ORCID http://orcid.org/0000-0003-2840-9791
Peter J ParkDepartment of Biomedical Informatics, Harvard Medical School, Boston, MA, 02115, USA. peter_park@hms.harvard.edu.ORCID http://orcid.org/0000-0001-9378-960X
Charles W M RobertsDepartment of Pediatric Oncology, Dana-Farber Cancer Institute, Boston, MA, 02215, USA. Charles.Roberts@STJUDE.ORG.
Dana-Farber Cancer Institute · USBroad Institute · USDartmouth College · USSt. Jude Children's Research Hospital · USHarvard University · US

Funding

Viral Vector Technology (VVTSR)P30CA021765 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI CHARLES ROBERTS · 1985 to 2026
$166.9M
Medical Scientist Training ProgramT32GM007753 · NIGMS · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI WALENSKY, LOREN DAVID · 1985 to 2021
$50.0M
The Dana-Farber Cancer Institute Cancer Target Discovery and Development CenterU01CA176058 · NCI · DANA-FARBER CANCER INST · PI HAHN, WILLIAM C. · 2013 to 2021
$7.8M
THE FUNCTION OF SNF5 (SMARCB1), AN EPIGENETIC TUMOR SUPPRESSORR01CA113794 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI CHARLES ROBERTS · 2005 to 2026
$7.8M
Role of the SWI/SNF complex in tumor suppressionR01CA172152 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI CHARLES ROBERTS · 2013 to 2026
$5.1M
Role of SNF5 in regulating SWI/SNF complex assembly & targeting in rhabdoid tumorR00CA197640 · NCI · DARTMOUTH COLLEGE · PI WANG, XIAOFENG · 2018 to 2020
$713k
Role of SNF5 in regulating SWI/SNF complex assembly & targeting in rhabdoid tumorK99CA197640 · NCI · DANA-FARBER CANCER INST · PI WANG, XIAOFENG · 2016 to 2017
$303k
NCI NIH HHS K99 CA197640NCI NIH HHS P30 CA021765NCI NIH HHS R00 CA197640NCI NIH HHS R01 CA113794NCI NIH HHS R01 CA172152NCI NIH HHS U01 CA176058NIGMS NIH HHS T32 GM007753
6 · The paper itself

Abstract

Bromodomain-containing protein 9 (BRD9) is a recently identified subunit of SWI/SNF(BAF) chromatin remodeling complexes, yet its function is poorly understood. Here, using a genome-wide CRISPR-Cas9 screen, we show that BRD9 is a specific vulnerability in pediatric malignant rhabdoid tumors (RTs), which are driven by inactivation of the SMARCB1 subunit of SWI/SNF. We find that BRD9 exists in a unique SWI/SNF sub-complex that lacks SMARCB1, which has been considered a core subunit. While SMARCB1-containing SWI/SNF complexes are bound preferentially at enhancers, we show that BRD9-containing complexes exist at both promoters and enhancers. Mechanistically, we show that SMARCB1 loss causes increased BRD9 incorporation into SWI/SNF thus providing insight into BRD9 vulnerability in RTs. Underlying the dependency, while its bromodomain is dispensable, the DUF3512 domain of BRD9 is essential for SWI/SNF integrity in the absence of SMARCB1. Collectively, our results reveal a BRD9-containing SWI/SNF subcomplex is required for the survival of SMARCB1-mutant RTs.

Indexed as

Chromatin Assembly and DisassemblyBromodomain Containing ProteinsCell Line, TumorCRISPR-Cas SystemsEnhancer Elements, GeneticGene Knockdown TechniquesGene Knockout TechniquesHumansMutationPromoter Regions, GeneticProtein DomainsRhabdoid TumorRNA, Small InterferingSMARCB1 ProteinTranscription FactorsBRD9 protein, humanBromodomain Containing ProteinsRNA, Small InterferingSMARCB1 ProteinSMARCB1 protein, humanTranscription Factors

Identifiers

PMID31015438
PMCPMC6479050
OpenAlexW2941269293

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.