Evidence map›Paper›PMID 38390898›Full record

ReviewEpigenomes2024

Targeting SWI/SNF Complexes in Cancer: Pharmacological Approaches and Implications.

Megan R Dreier, Jasmine Walia, Ivana L de la Serna

Open access · diamondAbstract readReview
In one paragraph

Review in Epigenomes, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
7.5field-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

22 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
  2. Article
  3. Targeting the Epigenome in Colorectal Cancer.International journal of molecular sciences · 2026
    Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Review
  16. Article
  17. Review
  18. Review
  19. Epigenetics-targeted drugs: current paradigms and future challenges.Signal transduction and targeted therapy · 2024
    Review
  20. Muscle-specific pyruvate kinase isoforms, PKM1 and PKM2, regulate mammalian SWI/SNF proteins and histone 3 phosphorylation during myoblast differentiation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
    Article
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

3 authors at 1 institution in 1 country.

Megan R DreierDepartment of Cell and Cancer Biology, University of Toledo College of Medicine and Life Sciences, 3000 Arlington Ave, Toledo 43614, OH, USA.
Jasmine WaliaDepartment of Cell and Cancer Biology, University of Toledo College of Medicine and Life Sciences, 3000 Arlington Ave, Toledo 43614, OH, USA.
Ivana L de la SernaDepartment of Cell and Cancer Biology, University of Toledo College of Medicine and Life Sciences, 3000 Arlington Ave, Toledo 43614, OH, USA.ORCID 0000-0002-6429-287X
University of Toledo · US

Funding

Melanoma Research Foundation Established Investigator Award
6 · The paper itself

Abstract

SWI/SNF enzymes are heterogeneous multi-subunit complexes that utilize the energy from ATP hydrolysis to remodel chromatin structure, facilitating transcription, DNA replication, and repair. In mammalian cells, distinct sub-complexes, including cBAF, ncBAF, and PBAF exhibit varying subunit compositions and have different genomic functions. Alterations in the SWI/SNF complex and sub-complex functions are a prominent feature in cancer, making them attractive targets for therapeutic intervention. Current strategies in cancer therapeutics involve the use of pharmacological agents designed to bind and disrupt the activity of SWI/SNF complexes or specific sub-complexes. Inhibitors targeting the catalytic subunits, SMARCA4/2, and small molecules binding SWI/SNF bromodomains are the primary approaches for suppressing SWI/SNF function. Proteolysis-targeting chimeras (PROTACs) were generated by the covalent linkage of the bromodomain or ATPase-binding ligand to an E3 ligase-binding moiety. This engineered connection promotes the degradation of specific SWI/SNF subunits, enhancing and extending the impact of this pharmacological intervention in some cases. Extensive preclinical studies have underscored the therapeutic potential of these drugs across diverse cancer types. Encouragingly, some of these agents have progressed from preclinical research to clinical trials, indicating a promising stride toward the development of effective cancer therapeutics targeting SWI/SNF complex and sub-complex functions.

Indexed as

allosteric ATPAse inhibitorsbromodomain inhibitorscancerDNA damageepigeneticsPROTACsSWI/SNF chromatin-remodeling complexestranscription

Identifiers

PMID38390898
PMCPMC10885108
OpenAlexW4391577102

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.