Evidence map›Paper›PMID 35468497›Full record

ArticleDNA repair2022

BCL-3 loss sensitises colorectal cancer cells to DNA damage by targeting homologous recombination.

Christopher Parker, Adam C Chambers, Dustin J Flanagan, Jasmine Wing Yu Ho, Tracey J Collard, Greg Ngo, Duncan M Baird, Penny Timms, Rhys G Morgan, Owen J Sansom and 1 more

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in DNA repair, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.6field-weighted citation impact, top 37% 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

6 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Article
  3. A Critical Role of DC-SIGNImmunoTargets and therapy · 2025
    Article
  4. Review
  5. Article
  6. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 5 institutions in 2 countries.

Christopher ParkerColorectal Tumour Biology Group, School of Cellular and Molecular Medicine, Faculty of Life Sciences, Biomedical Sciences Building, University Walk, University of Bristol, Bristol BS8 1TD, UK.
Adam C ChambersColorectal Tumour Biology Group, School of Cellular and Molecular Medicine, Faculty of Life Sciences, Biomedical Sciences Building, University Walk, University of Bristol, Bristol BS8 1TD, UK. Electronic address: adam.chambers@bristol.ac.uk.
Dustin J FlanaganCancer Research UK Beatson Institute, Garscube Estate, Switchback Road, Bearsden, Glasgow G61 1BD UK; Biomedicine Discovery Institute, Monash University, Melbourne 3800, Australia.
Jasmine Wing Yu HoCancer Research UK Beatson Institute, Garscube Estate, Switchback Road, Bearsden, Glasgow G61 1BD UK.
Tracey J CollardColorectal Tumour Biology Group, School of Cellular and Molecular Medicine, Faculty of Life Sciences, Biomedical Sciences Building, University Walk, University of Bristol, Bristol BS8 1TD, UK.
Greg NgoDivision of Cancer and Genetics, School of Medicine, Cardiff University, Cardiff CF14 4XN UK.
Duncan M BairdDivision of Cancer and Genetics, School of Medicine, Cardiff University, Cardiff CF14 4XN UK.
Penny TimmsColorectal Tumour Biology Group, School of Cellular and Molecular Medicine, Faculty of Life Sciences, Biomedical Sciences Building, University Walk, University of Bristol, Bristol BS8 1TD, UK.
Rhys G MorganSchool of Life Sciences, University of Sussex, Sussex House, Falmer, Brighton BN1 9RH UK.
Owen J SansomCancer Research UK Beatson Institute, Garscube Estate, Switchback Road, Bearsden, Glasgow G61 1BD UK.
Ann C WilliamsColorectal Tumour Biology Group, School of Cellular and Molecular Medicine, Faculty of Life Sciences, Biomedical Sciences Building, University Walk, University of Bristol, Bristol BS8 1TD, UK. Electronic address: Ann.C.Williams@bristol.ac.uk.
University of Bristol · GBCancer Research UK Scotland Institute · GBCardiff University · GBCancer Research UK · GBUniversity of Sussex · GB

Funding

Cancer Research UK 29202Cancer Research UK A18246/A29202Medical Research Council MR/N001494/1Medical Research Council MR/R017247/1Wellcome Trust 203988/Z/16/Z
6 · The paper itself

Abstract

The proto-oncogene BCL-3 is upregulated in a subset of colorectal cancers (CRC), where it has been shown to enhance tumour cell survival. However, although increased expression correlates with poor patient prognosis, the role of BCL-3 in determining therapeutic response remains largely unknown. In this study, we use combined approaches in multiple cell lines and pre-clinical mouse models to investigate the function of BCL-3 in the DNA damage response. We show that suppression of BCL-3 increases γH2AX foci formation and decreases homologous recombination in CRC cells, resulting in reduced RAD51 foci number and increased sensitivity to PARP inhibition. Importantly, a similar phenotype is seen in Bcl3

Indexed as

Colorectal NeoplasmsAnimalsCell Line, TumorCisplatinDNA DamageHomologous RecombinationHumansMiceCisplatinColorectal cancer/DNA Damage response/Therapy response/Chemoradiotherapy/Homologous recombination

Identifiers

PMID35468497
PMCPMC10618080
OpenAlexW4224077265

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.