Evidence map›Paper›PMID 39741332›Full record

ArticleGenome biology2024

Molecular dependencies and genomic consequences of a global DNA damage tolerance defect.

Daniel de Groot, Aldo Spanjaard, Ronak Shah, Maaike Kreft, Ben Morris, Cor Lieftink, Joyce J I Catsman, Shirley Ormel, Matilda Ayidah, Bas Pilzecker and 4 more

Abstract read
In one paragraph

Article in Genome biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. 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

14 authors.

Daniel de GrootDivision of Tumor Biology & Immunology, The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX, Amsterdam, The Netherlands.
Aldo SpanjaardDivision of Tumor Biology & Immunology, The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX, Amsterdam, The Netherlands.
Ronak ShahDivision of Tumor Biology & Immunology, The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX, Amsterdam, The Netherlands.
Maaike KreftDivision of Tumor Biology & Immunology, The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX, Amsterdam, The Netherlands.
Ben MorrisDivision of Molecular Carcinogenesis, The NKI Robotics and Screening Center, The Netherlands Cancer Institute, Plesmanlaan 121, 1066CX, Amsterdam, The Netherlands.
Cor LieftinkDivision of Molecular Carcinogenesis, The NKI Robotics and Screening Center, The Netherlands Cancer Institute, Plesmanlaan 121, 1066CX, Amsterdam, The Netherlands.
Joyce J I CatsmanDivision of Tumor Biology & Immunology, The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX, Amsterdam, The Netherlands.
Shirley OrmelDivision of Tumor Biology & Immunology, The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX, Amsterdam, The Netherlands.
Matilda AyidahDivision of Tumor Biology & Immunology, The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX, Amsterdam, The Netherlands.
Bas PilzeckerDivision of Tumor Biology & Immunology, The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX, Amsterdam, The Netherlands.
Olimpia Alessandra BuoninfanteDivision of Tumor Biology & Immunology, The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX, Amsterdam, The Netherlands.
Paul C M van den BerkDivision of Tumor Biology & Immunology, The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX, Amsterdam, The Netherlands.
Roderick L BeijersbergenDivision of Molecular Carcinogenesis, The NKI Robotics and Screening Center, The Netherlands Cancer Institute, Plesmanlaan 121, 1066CX, Amsterdam, The Netherlands.
Heinz JacobsDivision of Tumor Biology & Immunology, The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX, Amsterdam, The Netherlands. h.jacobs@nki.nl.ORCID 0000-0001-6227-9850

Funding

KWF Kankerbestrijding 10032KWF Kankerbestrijding 10796
6 · The paper itself

Abstract

backgroundDNA damage tolerance (DDT) enables replication to continue in the presence of fork stalling lesions. In mammalian cells, DDT is regulated by two independent pathways, controlled by the polymerase REV1 and ubiquitinated PCNA, respectively.

resultsTo determine the molecular and genomic impact of a global DDT defect, we studied Pcna

conclusionsOur data highlight the essential contribution of the DDT system to genome maintenance and type 3 deletions as mutational signature of replication stress. The unique characteristics of type 3 deletions implicate the existence of a novel deletion pathway in mice and humans that is counteracted by DDT.

Indexed as

DNA DamageDNA ReplicationNucleotidyltransferasesProliferating Cell Nuclear AntigenAnimalsDNA Damage ToleranceDNA-Directed DNA PolymeraseGenomic InstabilityHumansMiceSequence DeletionY-Family DNA PolymerasesDNA-Directed DNA PolymeraseNucleotidyltransferasesProliferating Cell Nuclear AntigenRev1 protein, mouseY-Family DNA Polymerases

Identifiers

PMID39741332
PMCPMC11687044

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.