Evidence map›Paper›PMID 39014081›Full record

ReviewNature reviews. Drug discovery2024

Chromatin remodellers as therapeutic targets.

Hayden A Malone, Charles W M Roberts

Abstract readReview
In one paragraph

Review in Nature reviews. Drug discovery, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed
–field-weighted citation impact
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

69 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Tuning epigenetics to enhance cancer virotherapy.Acta pharmaceutica Sinica. B · 2026
    Review
  5. Review
  6. Review
  7. Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Molecular Acrobats: How CHD Remodelers Shape the Genetic Playground to License Cell Identity.BioEssays : news and reviews in molecular, cellular and developmental biology · 2026
    Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. JACS Au · 2026
    Article
  20. Article

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

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

Hayden A MaloneDivision of Molecular Oncology, Department of Oncology, and Comprehensive Cancer Center, St. Jude Children's Research Hospital, Memphis, TN, USA.ORCID 0000-0002-0537-797X
Charles W M RobertsDivision of Molecular Oncology, Department of Oncology, and Comprehensive Cancer Center, St. Jude Children's Research Hospital, Memphis, TN, USA. charles.roberts@stjude.org.ORCID 0000-0003-1135-1896

Funding

Viral Vector Technology (VVTSR)P30CA021765 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI Shondra Michelle Miller · 1985 to 2026
$166.9M
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
Cancer-based discovery of novel mechanisms of chromatin controlR01CA273455 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI CHARLES ROBERTS · 2023 to 2026
$1.6M
Investigating essential chromatin regulators in cancers with SWI/SNF mutationsF31CA278355 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL GRADUATE SCHOOL OF BIOMEDICAL SCIENCES, LLC · PI MALONE, HAYDEN ABIGAIL · 2023 to 2025
$134k
Mechanistic Studies of a Novel Vulnerability in Pediatric CancerF31CA261150 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL GRADUATE SCHOOL OF BIOMEDICAL SCIENCES, LLC · PI RADKO-JUETTNER, SANDI · 2021 to 2022
$87k
NCI NIH HHS F31 CA261150NCI NIH HHS F31 CA278355NCI NIH HHS P30 CA021765NCI NIH HHS R01 CA113794NCI NIH HHS R01 CA172152NCI NIH HHS R01 CA273455
6 · The paper itself

Abstract

Large-scale cancer genome sequencing studies have revealed that chromatin regulators are frequently mutated in cancer. In particular, more than 20% of cancers harbour mutations in genes that encode subunits of SWI/SNF (BAF) chromatin remodelling complexes. Additional links of SWI/SNF complexes to disease have emerged with the findings that some oncogenes drive transformation by co-opting SWI/SNF function and that germline mutations in select SWI/SNF subunits are the basis of several neurodevelopmental disorders. Other chromatin remodellers, including members of the ISWI, CHD and INO80/SWR complexes, have also been linked to cancer and developmental disorders. Consequently, therapeutic manipulation of SWI/SNF and other remodelling complexes has become of great interest, and drugs that target SWI/SNF subunits have entered clinical trials. Genome-wide perturbation screens in cancer cell lines with SWI/SNF mutations have identified additional synthetic lethal targets and led to further compounds in clinical trials, including one that has progressed to FDA approval. Here, we review the progress in understanding the structure and function of SWI/SNF and other chromatin remodelling complexes, mechanisms by which SWI/SNF mutations cause cancer and neurological diseases, vulnerabilities that arise because of these mutations and efforts to target SWI/SNF complexes and synthetic lethal targets for therapeutic benefit.

Indexed as

Chromatin Assembly and DisassemblyNeoplasmsAnimalsAntineoplastic AgentsChromosomal Proteins, Non-HistoneHumansMolecular Targeted TherapyMutationTranscription FactorsAntineoplastic AgentsChromosomal Proteins, Non-HistoneTranscription Factors

Identifiers

PMID39014081
PMCPMC11534152

What OpenQuestion holds

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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.