Evidence map›Paper›PMID 33920223›Full record

ReviewInternational journal of molecular sciences2021

Translesion Synthesis or Repair by Specialized DNA Polymerases Limits Excessive Genomic Instability upon Replication Stress.

Domenico Maiorano, Jana El Etri, Camille Franchet, Jean-Sébastien Hoffmann

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.6field-weighted citation impact, top 9% 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

26 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Patterns of spontaneous and induced genomic alterations inApplied and environmental microbiology · 2025
    Article
  10. eLife · 2024
    Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. ISG15: A link between innate immune signaling, DNA replication, and genome stability.BioEssays : news and reviews in molecular, cellular and developmental biology · 2023
    Review
  17. Review
  18. Article
  19. Article
  20. Review
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

4 authors at 2 institutions in 1 country.

Domenico MaioranoInstitute of Human Genetics, UMR9002, CNRS-University of Montpellier, 34396 Montpellier, France.ORCID 0000-0003-4229-5903
Jana El EtriInstitute of Human Genetics, UMR9002, CNRS-University of Montpellier, 34396 Montpellier, France.
Camille FranchetLaboratoire D'Excellence Toulouse Cancer (TOUCAN), Laboratoire de Pathologie, Institut Universitaire du Cancer-Toulouse, Oncopole, 1 Avenue Irène-Joliot-Curie, 31059 Toulouse, France.
Jean-Sébastien HoffmannLaboratoire D'Excellence Toulouse Cancer (TOUCAN), Laboratoire de Pathologie, Institut Universitaire du Cancer-Toulouse, Oncopole, 1 Avenue Irène-Joliot-Curie, 31059 Toulouse, France.ORCID 0000-0003-2222-354X
Centre National de la Recherche Scientifique · FRInstitut universitaire du cancer de Toulouse Oncopole · FR

Funding

Fondation ARC pour la Recherche sur le Cancer to DMLABEX TOUCAN to JSHWorldwide Cancer Research 20-0120
6 · The paper itself

Abstract

DNA can experience "replication stress", an important source of genome instability, induced by various external or endogenous impediments that slow down or stall DNA synthesis. While genome instability is largely documented to favor both tumor formation and heterogeneity, as well as drug resistance, conversely, excessive instability appears to suppress tumorigenesis and is associated with improved prognosis. These findings support the view that karyotypic diversity, necessary to adapt to selective pressures, may be limited in tumors so as to reduce the risk of excessive instability. This review aims to highlight the contribution of specialized DNA polymerases in limiting extreme genetic instability by allowing DNA replication to occur even in the presence of DNA damage, to either avoid broken forks or favor their repair after collapse. These mechanisms and their key regulators Rad18 and Polθ not only offer diversity and evolutionary advantage by increasing mutagenic events, but also provide cancer cells with a way to escape anti-cancer therapies that target replication forks.

Indexed as

DNA-Binding ProteinsDNA DamageDNA-Directed DNA PolymeraseDNA Polymerase thetaDNA RepairDNA ReplicationGenomic InstabilityHumansMutagenesisNeoplasmsUbiquitin-Protein LigasesDNA-Binding ProteinsDNA-Directed DNA PolymeraseDNA Polymerase thetaRAD18 protein, humanUbiquitin-Protein LigasesDSB repairgenome instabilityPOLQPol thetareplicative stressspecialized DNA polymerasesTMEJtranslesion synthesis (TLS), Rad18

Identifiers

PMID33920223
PMCPMC8069355
OpenAlexW3154855069

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.