Evidence map›Paper›PMID 28967863›Full record

ArticleeLife2017

Chromatin accessibility underlies synthetic lethality of SWI/SNF subunits in ARID1A-mutant cancers.

Timothy W R Kelso, Devin K Porter, Maria Luisa Amaral, Maxim N Shokhirev, Christopher Benner, Diana C Hargreaves

Abstract read
In one paragraph

Article in eLife, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 120 papers.

0numbers the graph read from it
0cells of the map it votes in
120citing 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

120 citing papers in PubMed.

  1. Tuning epigenetics to enhance cancer virotherapy.Acta pharmaceutica Sinica. B · 2026
    Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article

60 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

6 authors.

Timothy W R KelsoMolecular and Cell Biology Laboratory, Salk Institute for Biological Studies, California, United States.
Devin K PorterMolecular and Cell Biology Laboratory, Salk Institute for Biological Studies, California, United States.
Maria Luisa AmaralThe Razavi Newman Integrative Genomics and Bioinformatics Core Facility, Salk Institute for Biological Studies, California, United States.
Maxim N ShokhirevThe Razavi Newman Integrative Genomics and Bioinformatics Core Facility, Salk Institute for Biological Studies, California, United States.
Christopher BennerDepartment of Medicine, University of California San Diego, California, United States.
Diana C HargreavesMolecular and Cell Biology Laboratory, Salk Institute for Biological Studies, California, United States.ORCID http://orcid.org/0000-0003-3724-3826

Funding

Epigenetic regulation of embryonic stem cells by ATP-dependent BAF chromatin remodeling complexesR35GM128943 · NIGMS · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI HARGREAVES, DIANA CLARE · 2018 to 2022
$2.5M
Targeting Ovarian Cancer via Cooperative Oncogene InteractionsR00CA184043 · NCI · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI HARGREAVES, DIANA CLARE · 2015 to 2017
$747k
NCI NIH HHS R00 CA184043NIGMS NIH HHS R35 GM128943
6 · The paper itself

Abstract

ARID1A, a subunit of the SWI/SNF chromatin remodeling complex, is frequently mutated in cancer. Deficiency in its homolog ARID1B is synthetically lethal with ARID1A mutation. However, the functional relationship between these homologs has not been explored. Here, we use ATAC-seq, genome-wide histone modification mapping, and expression analysis to examine colorectal cancer cells lacking one or both ARID proteins. We find that ARID1A has a dominant role in maintaining chromatin accessibility at enhancers, while the contribution of ARID1B is evident only in the context of ARID1A mutation. Changes in accessibility are predictive of changes in expression and correlate with loss of H3K4me and H3K27ac marks, nucleosome spacing, and transcription factor binding, particularly at growth pathway genes including

Indexed as

Synthetic Lethal MutationsCell Line, TumorChromatinDNA-Binding ProteinsHistonesHumansMutant ProteinsNeoplasmsNuclear ProteinsProtein Processing, Post-TranslationalTranscription FactorsARID1A protein, humanARID1B protein, humanChromatinDNA-Binding ProteinsHistonesMutant ProteinsNuclear ProteinsTranscription FactorsARID1AARID1Bchromatin accessibilitychromatin remodelingchromosomesepigeneticsgeneshumanSWI/SNF complex

Identifiers

PMID28967863
PMCPMC5643100

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.