Evidence map›Paper›PMID 36810086›Full record

ReviewMolecular cancer2023

SWI/SNF complexes in hematological malignancies: biological implications and therapeutic opportunities.

Alvaro Andrades, Paola Peinado, Juan Carlos Alvarez-Perez, Juan Sanjuan-Hidalgo, Daniel J García, Alberto M Arenas, Ana M Matia-González, Pedro P Medina

Open access · goldAbstract readReview
In one paragraph

Review in Molecular cancer, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 2 pooled it
9.8field-weighted citation impact, top 1% 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

43 citing papers in PubMed, 2 syntheses or guidelines pooled it, 62 citations in OpenAlex.

  1. Pooled it
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  12. BRD9 at the crossroads of splicing, chromatin remodeling, and hematopoiesis.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2026
    Review
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  17. Arid2 promotes Follicular B-cell differentiation and antibody responsesbioRxiv : the preprint server for biology · 2025
    Article
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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

8 authors at 3 institutions in 2 countries.

Alvaro Andrades *Department of Biochemistry and Molecular Biology I. Faculty of Sciences, University of Granada, Granada, Spain.
Paola Peinado *Department of Biochemistry and Molecular Biology I. Faculty of Sciences, University of Granada, Granada, Spain.
Juan Carlos Alvarez-Perez *Department of Biochemistry and Molecular Biology I. Faculty of Sciences, University of Granada, Granada, Spain.
Juan Sanjuan-HidalgoDepartment of Biochemistry and Molecular Biology I. Faculty of Sciences, University of Granada, Granada, Spain.
Daniel J GarcíaGENYO, Centre for Genomics and Oncological Research: Pfizer/University of Granada/Andalusian Regional Government, PTS Granada, Granada, Spain.
Alberto M ArenasDepartment of Biochemistry and Molecular Biology I. Faculty of Sciences, University of Granada, Granada, Spain.
Ana M Matia-GonzálezDepartment of Biochemistry and Molecular Biology I. Faculty of Sciences, University of Granada, Granada, Spain.
Pedro P MedinaDepartment of Biochemistry and Molecular Biology I. Faculty of Sciences, University of Granada, Granada, Spain. pedromedina@ugr.es.
Universidad de Granada · ESPfizer-University of Granada-Junta de Andalucía Centre for Genomics and Oncological Research · ESInstituto de Investigación Biosanitaria de Granada · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hematological malignancies are a highly heterogeneous group of diseases with varied molecular and phenotypical characteristics. SWI/SNF (SWItch/Sucrose Non-Fermentable) chromatin remodeling complexes play significant roles in the regulation of gene expression, being essential for processes such as cell maintenance and differentiation in hematopoietic stem cells. Furthermore, alterations in SWI/SNF complex subunits, especially in ARID1A/1B/2, SMARCA2/4, and BCL7A, are highly recurrent across a wide variety of lymphoid and myeloid malignancies. Most genetic alterations cause a loss of function of the subunit, suggesting a tumor suppressor role. However, SWI/SNF subunits can also be required for tumor maintenance or even play an oncogenic role in certain disease contexts. The recurrent alterations of SWI/SNF subunits highlight not only the biological relevance of SWI/SNF complexes in hematological malignancies but also their clinical potential. In particular, increasing evidence has shown that mutations in SWI/SNF complex subunits confer resistance to several antineoplastic agents routinely used for the treatment of hematological malignancies. Furthermore, mutations in SWI/SNF subunits often create synthetic lethality relationships with other SWI/SNF or non-SWI/SNF proteins that could be exploited therapeutically. In conclusion, SWI/SNF complexes are recurrently altered in hematological malignancies and some SWI/SNF subunits may be essential for tumor maintenance. These alterations, as well as their synthetic lethal relationships with SWI/SNF and non-SWI/SNF proteins, may be pharmacologically exploited for the treatment of diverse hematological cancers.

Indexed as

Antineoplastic AgentsHematologic NeoplasmsNeoplasmsGenes, Tumor SuppressorHumansMutationAntineoplastic AgentsBAF complexesChromatin remodelingDrug resistanceEpigeneticsLeukemiaLymphomaMultiple myelomaSWI/SNFSynthetic lethality

Identifiers

PMID36810086
PMCPMC9942420
OpenAlexW4321457539

What Socratic 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 Socratic graph.