Evidence map›Paper›PMID 31796878›Full record

ArticleScientific reports2019

Targeting ARID1A-mutant colorectal cancer: depletion of ARID1B increases radiosensitivity and modulates DNA damage response.

B Niedermaier, A Sak, E Zernickel, Shan Xu, M Groneberg, M Stuschke

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

20 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Article
  3. The Role of SWI/SNF Complex in Bladder Cancer.Journal of cellular and molecular medicine · 2025
    Review
  4. The role of SWI/SNF complexes in digestive system neoplasms.Medical oncology (Northwood, London, England) · 2024
    Review
  5. Article
  6. Phase I Study and Cell-Free DNA Analysis of T-DM1 and Metronomic Temozolomide for Secondary Prevention of HER2-Positive Breast Cancer Brain Metastases.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023
    Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Oncometabolites and the response to radiotherapy.Radiation oncology (London, England) · 2020
    Review
  18. 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

6 authors at 2 institutions in 1 country.

B NiedermaierDepartment of Radiotherapy, University of Duisburg-Essen, University Hospital, Essen, Germany. benedikt.niedermaier@uk-essen.de.
A SakDepartment of Radiotherapy, University of Duisburg-Essen, University Hospital, Essen, Germany.
E ZernickelDepartment of Radiotherapy, University of Duisburg-Essen, University Hospital, Essen, Germany.
Shan XuDepartment of Radiotherapy, University of Duisburg-Essen, University Hospital, Essen, Germany.
M GronebergDepartment of Radiotherapy, University of Duisburg-Essen, University Hospital, Essen, Germany.
M StuschkeDepartment of Radiotherapy, University of Duisburg-Essen, University Hospital, Essen, Germany.
Essen University Hospital · DEUniversity of Duisburg-Essen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The SWI/SNF chromatin remodeling complex has been found mutated in a wide range of human cancers, causing alterations in gene expression patterns, proliferation and DNA damage response that have been linked to poor clinical prognosis. Here, we investigated weather knockdown of ARID1B, one of two mutually exclusive subunits within the SWI/SNF complex, can sensitize colorectal cancer cell lines mutated in the other subunit, ARID1A, to ionizing radiation (IR). ARID1A-mutated colorectal cancer (CRC) cell lines are selectively sensitized to IR after siRNA mediated ARID1B depletion, as measured by clonogenic survival. This is characterized by a decrease in the surviving cell fraction to 87.3% ± 2.1%, 86.0% ± 1.1% and 77.2% ± 1.5% per 1 Gy compared with control siRNA exposed cells in the dose range of 0-6 Gy for the LS180, RKO and SW48 lines, respectively (p < 0.0001, F-test). The magnitude of this dose modifying effect was significantly larger in ARID1A mutated than in non-mutated cell lines (Spearman rank correlation rs = 0.88, p = 0.02). Furthermore, initial formation of RAD51 foci at 4 h after IR, as a measure for homologous recombination repair, was significantly reduced in ARID1A-mutant CRC cell lines but not in the majority of wildtype lines nor in fibroblasts. These findings open up perspectives for targeting ARID1B in combination with radiotherapy to improve outcomes of patients with ARID1A-mutant CRC.

Indexed as

Antineoplastic AgentsCell Line, TumorChemoradiotherapyChromatin Assembly and DisassemblyColorectal NeoplasmsDNA-Binding ProteinsDNA Breaks, Double-StrandedDNA RepairGene Knockdown TechniquesHumansMutationRad51 RecombinaseRadiation ToleranceRNA, Small InterferingTranscription FactorsTumor Stem Cell AssayAntineoplastic AgentsARID1A protein, humanARID1B protein, humanDNA-Binding ProteinsRAD51 protein, humanRad51 RecombinaseRNA, Small InterferingTP53BP1 protein, humanTranscription FactorsTumor Suppressor p53-Binding Protein 1

Identifiers

PMID31796878
PMCPMC6890697
OpenAlexW2991681839

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.