Evidence map›Paper›PMID 34638302›Full record

ReviewCancers2021

Beyond the Double-Strand Breaks: The Role of DNA Repair Proteins in Cancer Stem-Cell Regulation.

Jacqueline Nathansen, Felix Meyer, Luise Müller, Marc Schmitz, Kerstin Borgmann, Anna Dubrovska

Open access · goldAbstract readReview
In one paragraph

Review in Cancers, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing 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

29 citing papers in PubMed, 42 citations in OpenAlex.

  1. Review
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  4. Current Perspectives on Radiosensitizers in Cancer Radiotherapy.International journal of nanomedicine · 2026
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  19. Eradicating the tumor "seeds": nanomedicines-based therapies against cancer stem cells.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2023
    Review
  20. 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

6 authors at 4 institutions in 1 country.

Jacqueline NathansenOncoRay-National Center for Radiation Research in Oncology, Faculty of Medicine and University Hospital Carl Gustav Carus, Technische Universität Dresden and Helmholtz-Zentrum Dresden-Rossendorf, 01309 Dresden, Germany.
Felix MeyerLaboratory of Radiobiology & Experimental Radiooncology, Department of Radiotherapy and Radiation Oncology, Center of Oncology, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany.
Luise MüllerInstitute of Immunology, Faculty of Medicine Carl Gustav Carus, TU Dresden, 01307 Dresden, Germany.ORCID 0000-0002-6610-326X
Marc SchmitzInstitute of Immunology, Faculty of Medicine Carl Gustav Carus, TU Dresden, 01307 Dresden, Germany.
Kerstin BorgmannLaboratory of Radiobiology & Experimental Radiooncology, Department of Radiotherapy and Radiation Oncology, Center of Oncology, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany.
Anna DubrovskaOncoRay-National Center for Radiation Research in Oncology, Faculty of Medicine and University Hospital Carl Gustav Carus, Technische Universität Dresden and Helmholtz-Zentrum Dresden-Rossendorf, 01309 Dresden, Germany.
German Cancer Research Center · DEUniversität Hamburg · DEHelmholtz-Zentrum Dresden-Rossendorf · DEUniversity Hospital Carl Gustav Carus · DE

Funding

Deutsche Forschungsgemeinschaft 416001651Deutsche Forschungsgemeinschaft SPP 2084: µBONE, 401326337Federal Ministry of Education and Research 02NUK035B
6 · The paper itself

Abstract

Cancer stem cells (CSCs) are pluripotent and highly tumorigenic cells that can re-populate a tumor and cause relapses even after initially successful therapy. As with tissue stem cells, CSCs possess enhanced DNA repair mechanisms. An active DNA damage response alleviates the increased oxidative and replicative stress and leads to therapy resistance. On the other hand, mutations in DNA repair genes cause genomic instability, therefore driving tumor evolution and developing highly aggressive CSC phenotypes. However, the role of DNA repair proteins in CSCs extends beyond the level of DNA damage. In recent years, more and more studies have reported the unexpected role of DNA repair proteins in the regulation of transcription, CSC signaling pathways, intracellular levels of reactive oxygen species (ROS), and epithelial-mesenchymal transition (EMT). Moreover, DNA damage signaling plays an essential role in the immune response towards tumor cells. Due to its high importance for the CSC phenotype and treatment resistance, the DNA damage response is a promising target for individualized therapies. Furthermore, understanding the dependence of CSC on DNA repair pathways can be therapeutically exploited to induce synthetic lethality and sensitize CSCs to anti-cancer therapies. This review discusses the different roles of DNA repair proteins in CSC maintenance and their potential as therapeutic targets.

Indexed as

cancer stem cellscancer therapyDNA repairgenomic instabilityimmune responseoxidative stressreplicative stressreprogramming

Identifiers

PMID34638302
PMCPMC8508278
OpenAlexW3204917837

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.