Evidence map›Paper›PMID 25852742›Full record

ReviewFrontiers in genetics2015

Regulators of homologous recombination repair as novel targets for cancer treatment.

Małgorzata Krajewska, Rudolf S N Fehrmann, Elisabeth G E de Vries, Marcel A T M van Vugt

Abstract readReview
In one paragraph

Review in Frontiers in genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 1 pooled it
–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

47 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Trial
  3. Article
  4. Article
  5. Review
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  7. Review
  8. Antitumoral Activity of the Universal Methyl DonorMolecules (Basel, Switzerland) · 2024
    Article
  9. DNA damage and repair: underlying mechanisms leading to microcephaly.Frontiers in cell and developmental biology · 2023
    Review
  10. Association of variations in theFrontiers in pharmacology · 2023
    Article
  11. Article
  12. Article
  13. Recent Insights into PARP and Immuno-Checkpoint Inhibitors in Epithelial Ovarian Cancer.International journal of environmental research and public health · 2022
    Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
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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.

Małgorzata KrajewskaDepartment of Medical Oncology, Cancer Research Center Groningen, University Medical Center Groningen, University of Groningen Groningen, Netherlands.
Rudolf S N FehrmannDepartment of Medical Oncology, Cancer Research Center Groningen, University Medical Center Groningen, University of Groningen Groningen, Netherlands.
Elisabeth G E de VriesDepartment of Medical Oncology, Cancer Research Center Groningen, University Medical Center Groningen, University of Groningen Groningen, Netherlands.
Marcel A T M van VugtDepartment of Medical Oncology, Cancer Research Center Groningen, University Medical Center Groningen, University of Groningen Groningen, Netherlands.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To cope with DNA damage, cells possess a complex signaling network called the 'DNA damage response', which coordinates cell cycle control with DNA repair. The importance of this network is underscored by the cancer predisposition that frequently goes along with hereditary mutations in DNA repair genes. One especially important DNA repair pathway in this respect is homologous recombination (HR) repair. Defects in HR repair are observed in various cancers, including hereditary breast, and ovarian cancer. Intriguingly, tumor cells with defective HR repair show increased sensitivity to chemotherapeutic reagents, including platinum-containing agents. These observations suggest that HR-proficient tumor cells might be sensitized to chemotherapeutics if HR repair could be therapeutically inactivated. HR repair is an extensively regulated process, which depends strongly on the activity of various other pathways, including cell cycle pathways, protein-control pathways, and growth factor-activated receptor signaling pathways. In this review, we discuss how the mechanistic wiring of HR is controlled by cell-intrinsic or extracellular pathways. Furthermore, we have performed a meta-analysis on available genome-wide RNA interference studies to identify additional pathways that control HR repair. Finally, we discuss how these HR-regulatory pathways may provide therapeutic targets in the context of radio/chemosensitization.

Indexed as

Cell CycleDNA Repairgenomic instabilityPARP inhibitorsrecombination

Identifiers

PMID25852742
PMCPMC4367534

What OpenQuestion holds

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Registered trials

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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.