Evidence map›Paper›PMID 27596623›Full record

ArticleEMBO reports2016

Loss of CHD1 causes DNA repair defects and enhances prostate cancer therapeutic responsiveness.

Vijayalakshmi Kari, Wael Yassin Mansour, Sanjay Kumar Raul, Simon J Baumgart, Andreas Mund, Marian Grade, Hüseyin Sirma, Ronald Simon, Hans Will, Matthias Dobbelstein and 2 more

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in EMBO reports, 2016. 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 70 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed, 1 pooled it
6.6field-weighted citation impact, top 2% 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

70 citing papers in PubMed, 1 synthesis or guideline pooled it, 111 citations in OpenAlex.

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10 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 4 institutions in 3 countries.

Vijayalakshmi KariDepartment of General, Visceral and Pediatric Surgery, University Medical Center Göttingen, Göttingen, Germany vkari1@gwdg.de steven.johnsen@med.uni-goettingen.de.
Wael Yassin MansourDepartment of Tumor Biology, National Cancer Institute, Cairo University, Cairo, Egypt.
Sanjay Kumar RaulDepartment of General, Visceral and Pediatric Surgery, University Medical Center Göttingen, Göttingen, Germany.
Simon J BaumgartDepartment of General, Visceral and Pediatric Surgery, University Medical Center Göttingen, Göttingen, Germany.
Andreas MundChromatin Structure and Function Group, Protein Signaling Program, The Novo Nordisk Foundation Center for Protein Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.
Marian GradeDepartment of General, Visceral and Pediatric Surgery, University Medical Center Göttingen, Göttingen, Germany.
Hüseyin SirmaInstitute of Pathology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Ronald SimonInstitute of Pathology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Hans WillInstitute for Tumor Biology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Matthias DobbelsteinInstitute of Molecular Oncology, University Medical Center Göttingen, Göttingen, Germany.
Ekkehard DikomeyInstitute of Pathology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Steven A JohnsenDepartment of General, Visceral and Pediatric Surgery, University Medical Center Göttingen, Göttingen, Germany vkari1@gwdg.de steven.johnsen@med.uni-goettingen.de.ORCID 0000-0003-1198-5805
Universitätsmedizin Göttingen · DEUniversität Hamburg · DECairo University · EGUniversity of Copenhagen · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The CHD1 gene, encoding the chromo-domain helicase DNA-binding protein-1, is one of the most frequently deleted genes in prostate cancer. Here, we examined the role of CHD1 in DNA double-strand break (DSB) repair in prostate cancer cells. We show that CHD1 is required for the recruitment of CtIP to chromatin and subsequent end resection during DNA DSB repair. Our data support a role for CHD1 in opening the chromatin around the DSB to facilitate the recruitment of homologous recombination (HR) proteins. Consequently, depletion of CHD1 specifically affects HR-mediated DNA repair but not non-homologous end joining. Together, we provide evidence for a previously unknown role of CHD1 in DNA DSB repair via HR and show that CHD1 depletion sensitizes cells to PARP inhibitors, which has potential therapeutic relevance. Our findings suggest that CHD1 deletion, like BRCA1/2 mutation in ovarian cancer, may serve as a marker for prostate cancer patient stratification and the utilization of targeted therapies such as PARP inhibitors, which specifically target tumors with HR defects.

Indexed as

DNA RepairBiomarkersCarrier ProteinsCell Line, TumorChromatinDNA-Binding ProteinsDNA Breaks, Double-StrandedDNA HelicasesEndodeoxyribonucleasesHumansMaleNuclear ProteinsPoly(ADP-ribose) Polymerase InhibitorsProstatic NeoplasmsRecombinational DNA RepairBiomarkersCarrier ProteinsCHD1 protein, humanChromatinDNA-Binding ProteinsDNA HelicasesEndodeoxyribonucleasesNuclear ProteinsPoly(ADP-ribose) Polymerase InhibitorsRBBP8 protein, humanCHD1chromatinDNA repairPARP inhibitorprostate cancer

Identifiers

PMID27596623
PMCPMC5090703
OpenAlexW2511945448

What OpenQuestion holds

Textmetadata
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.