Evidence map›Paper›PMID 25954303›Full record

ArticleFrontiers in genetics2015

DNA repair mechanisms in cancer development and therapy.

Alessandro Torgovnick, Björn Schumacher

Open access · goldAbstract read
In one paragraph

Article 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 197 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
197citing papers in PubMed, 1 pooled it
5.9field-weighted citation impact, top 3% 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

197 citing papers in PubMed, 1 synthesis or guideline pooled it, 391 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Review
  6. Advances in applications of siRNA in cancer therapy: challenges and opportunities.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Review
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  9. Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Recent patents on biotechnology · 2026
    Article
  15. Ubiquitin-conjugating Enzymes in Cancer.International journal of biological sciences · 2026
    Review
  16. Review
  17. The function of Mgs1/WRNIP1 in genome maintenance.Frontiers in molecular biosciences · 2026
    Review
  18. Article
  19. Pre-treatment with caffeic acid-phthalimide prevents UVB-induced oxidative stress and cytotoxicity.Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology · 2025
    Article
  20. Article

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

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

2 authors at 1 institution in 1 country.

Alessandro TorgovnickInstitute for Genome Stability in Ageing and Disease, Medical Faculty, University of Cologne , Cologne, Germany ; Cologne Excellence Cluster for Cellular Stress Responses in Aging-Associated Diseases Research Center, University of Cologne , Cologne, Germany ; Center for Molecular Medicine Cologne, University of Cologne , Cologne, Germany ; Systems Biology of Ageing Cologne, University of Cologne , Cologne, Germany.
Björn SchumacherInstitute for Genome Stability in Ageing and Disease, Medical Faculty, University of Cologne , Cologne, Germany ; Cologne Excellence Cluster for Cellular Stress Responses in Aging-Associated Diseases Research Center, University of Cologne , Cologne, Germany ; Center for Molecular Medicine Cologne, University of Cologne , Cologne, Germany ; Systems Biology of Ageing Cologne, University of Cologne , Cologne, Germany.
University of Cologne · DE

Funding

European Research Council 260383
6 · The paper itself

Abstract

DNA damage has been long recognized as causal factor for cancer development. When erroneous DNA repair leads to mutations or chromosomal aberrations affecting oncogenes and tumor suppressor genes, cells undergo malignant transformation resulting in cancerous growth. Genetic defects can predispose to cancer: mutations in distinct DNA repair systems elevate the susceptibility to various cancer types. However, DNA damage not only comprises a root cause for cancer development but also continues to provide an important avenue for chemo- and radiotherapy. Since the beginning of cancer therapy, genotoxic agents that trigger DNA damage checkpoints have been applied to halt the growth and trigger the apoptotic demise of cancer cells. We provide an overview about the involvement of DNA repair systems in cancer prevention and the classes of genotoxins that are commonly used for the treatment of cancer. A better understanding of the roles and interactions of the highly complex DNA repair machineries will lead to important improvements in cancer therapy.

Indexed as

agingataxia telangiectasiacancer therapyDNA repairFanconi anemiagenome instabilityprogeroid syndromesxeroderma pigmentosum

Identifiers

PMID25954303
PMCPMC4407582
OpenAlexW2073769648

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.