Evidence map›Paper›PMID 30986130›Full record

ReviewExpert review of anticancer therapy2019

Remodeling the cancer epigenome: mutations in the SWI/SNF complex offer new therapeutic opportunities.

Krystal A Orlando, Vinh Nguyen, Jesse R Raab, Tara Walhart, Bernard E Weissman

Open access · greenAbstract readReview
In one paragraph

Review in Expert review of anticancer therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

32 citing papers in PubMed, 51 citations in OpenAlex.

  1. Review
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  3. Review
  4. Article
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  8. Research progress on the role of the NEIL family in cancer.Frontiers in cell and developmental biology · 2025
    Review
  9. A Critical Review of the Impact ofJournal of personalized medicine · 2024
    Review
  10. Article
  11. Review
  12. Article
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  14. Review
  15. Article
  16. Article
  17. Article
  18. The Splicing Factor PTBP1 RepressesCancer research communications · 2022
    Article
  19. Review
  20. 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

5 authors at 2 institutions in 1 country.

Krystal A Orlandoa Department of Pathology and Laboratory Medicine , University of North Carolina , Chapel Hill , NC , USA.
Vinh Nguyenb Curriculum in Toxicology and Environmental Medicine , University of North Carolina , Chapel Hill , NC , USA.
Jesse R Raabc Department of Genetics , University of North Carolina , Chapel Hill , NC , USA.
Tara Walhartd Lineberger Comprehensive Cancer Center , University of North Carolina , Chapel Hill , NC , USA.
Bernard E Weissmana Department of Pathology and Laboratory Medicine , University of North Carolina , Chapel Hill , NC , USA.
University of North Carolina at Chapel Hill · USUNC Lineberger Comprehensive Cancer Center

Funding

TOXICOLOGYT32ES007126 · NIEHS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI ILONA JASPERS, Bernard E. Weissman · 1985 to 2026
$13.0M
The Tumor Suppressor Role of SMARCA4 in SCCOHTR01CA195670 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI HUNTSMAN, DAVID, TRENT, JEFFREY M. · 2015 to 2019
$3.7M
Cancer Epigenetics Training GrantT32CA217824 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI WEISSMAN, BERNARD E. · 2017 to 2021
$1.8M
NCI NIH HHS R01 CA195670NCI NIH HHS T32 CA217824NIEHS NIH HHS T32 ES007126
6 · The paper itself

Abstract

introductionCancer genome sequencing studies have discovered mutations in members of the SWItch/Sucrose Non-Fermentable (SWI/SNF) chromatin-remodeling complex in nearly 25% of human cancers. The SWI/SNF complex, first discovered in S. cerevisiae, shows strong conservation from yeast to Drosophila to mammals, contains approximately 10-12 subunits and regulates nucleosome positioning through the energy generated by its ATPase subunits. The unexpected finding of frequent mutations in the complex has fueled studies to identify the mechanisms that drive tumor development and the accompanying therapeutic vulnerabilities. Areas covered: In the review, we focus upon the potential roles different SWI/SNF subunit mutations play in human oncogenesis, their common and unique mechanisms of transformation and the potential for translating these mechanisms into targeted therapies for SWI/SNF-mutant tumors. Expert opinion: We currently have limited insights into how mutations in different SWI/SNF subunits drive the development of human tumors. Because the SWI/SNF complex participates in a broad range of normal cellular functions, defining specific oncogenic pathways has proved difficult. In addition, therapeutic options for SWI/SNF-mutant cancers have mainly evolved from high-throughput screens of cell lines with mutations in different subunits. Future studies should follow a more coherent plan to pinpoint common vulnerabilities among these tumors.

Indexed as

Molecular Targeted TherapyAnimalsCarcinogenesisChromosomal Proteins, Non-HistoneEpigenomeHigh-Throughput Screening AssaysHumansMutationNeoplasmsTranscription FactorsChromosomal Proteins, Non-HistoneSWI-SNF-B chromatin-remodeling complexTranscription FactorsCancerchromatin remodelingepigeneticsSWI/SNF complex

Identifiers

PMID30986130
PMCPMC6533634
OpenAlexW2937507204

What OpenQuestion holds

Textmetadata
LicenceTDM
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.