Evidence map›Paper›PMID 26773346›Full record

ReviewSeminars in cancer biology2016

Systemic DNA damage responses in aging and diseases.

Flavia Ribezzo, Yosef Shiloh, Björn Schumacher

Abstract readReview
In one paragraph

Review in Seminars in cancer biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed, 2 pooled it
8.9field-weighted citation impact, top 2% 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

64 citing papers in PubMed, 2 syntheses or guidelines pooled it, 119 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Reconstitution of genome remodeling usingFrontiers in cell and developmental biology · 2026
    Review
  5. Endothelial Nuclear and Cytoskeletal Responses to Mechanical Stresses.Advances in experimental medicine and biology · 2026
    Article
  6. From Genome to Geroscience: How DNA Damage Shapes Systemic Decline.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025
    Review
  7. ATR-CHK1 Axis Inhibitors in Gastric Cancer Treatment.International journal of molecular sciences · 2025
    Review
  8. Article
  9. Article
  10. Article
  11. Salubrious effects of proanthocyanidins on behavioral phenotypes and DNA repair deficiency in the BTBR mouse model of autism.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2024
    Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. Article

4 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

3 authors at 2 institutions in 2 countries.

Flavia RibezzoInstitute for Genome Stability in Ageing and Disease, Cologne Cluster of Excellence in Cellular Stress Responses in Aging-associated Diseases (CECAD) Research Center, Center for Molecular Medicine (CMMC), University of Cologne, Cologne, Germany.
Yosef ShilohThe David and Inez Myers Laboratory for Genetic Research, Department of Human Molecular Genetics and Biochemistry, Sackler School of Medicine, Tel Aviv University, Tel Aviv 69978, Israel.
Björn SchumacherInstitute for Genome Stability in Ageing and Disease, Cologne Cluster of Excellence in Cellular Stress Responses in Aging-associated Diseases (CECAD) Research Center, Center for Molecular Medicine (CMMC), University of Cologne, Cologne, Germany. Electronic address: bjoern.schumacher@uni-koeln.de.
University of Cologne · DETel Aviv University · IL

Funding

European Research Council 260383
6 · The paper itself

Abstract

The genome is constantly attacked by a variety of genotoxic insults. The causal role for DNA damage in aging and cancer is exemplified by genetic defects in DNA repair that underlie a broad spectrum of acute and chronic human disorders that are characterized by developmental abnormalities, premature aging, and cancer predisposition. The disease symptoms are typically tissue-specific with uncertain genotype-phenotype correlation. The cellular DNA damage response (DDR) has been extensively investigated ever since yeast geneticists discovered DNA damage checkpoint mechanisms, several decades ago. In recent years, it has become apparent that not only cell-autonomous but also systemic DNA damage responses determine the outcome of genome instability in organisms. Understanding the mechanisms of non-cell-autonomous DNA damage responses will provide important new insights into the role of genome instability in human aging and a host of diseases including cancer and might better explain the complex phenotypes caused by genome instability.

Indexed as

DNA DamageDNA RepairGenomic InstabilityAgingAnimalsCellular SenescenceDNA Breaks, Double-StrandedGenetic Association StudiesHumansImmunity, InnateMutationNeoplasmsAgingAtaxia-telangiectasia mutatedCancerDNA damage responseDNA repairNucleotide excision repairSystemic DNA damage response

Identifiers

PMID26773346
PMCPMC4886830
OpenAlexW2227508297

What OpenQuestion holds

Textmetadata
LicenceTDM
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.