Evidence map›Paper›PMID 20177397›Full record

ReviewNature reviews. Molecular cell biology2010

Genomic instability--an evolving hallmark of cancer.

Simona Negrini, Vassilis G Gorgoulis, Thanos D Halazonetis

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Molecular cell biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1,354 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
1,354citing papers in PubMed, 2 pooled it
53.4field-weighted citation impact, top 1% 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

1,354 citing papers in PubMed, 2 syntheses or guidelines pooled it, 2,355 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Causal graph neural networks for healthcare.Nature biomedical engineering · 2026
    Review
  16. The Prognostic Significance ofCurrent oncology (Toronto, Ont.) · 2026
    Article
  17. Review
  18. Review
  19. Review
  20. Combinatorial Delivery of Low-Dose Radiotherapy and Immunotherapy to Patients with Immune-Excluded Tumors Enhances CD8+ T-cell Functionality.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026
    Article

1,294 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.

Simona NegriniDepartment of Molecular Biology, CH-1205 Geneva, Switzerland.
Vassilis G Gorgoulis
Thanos D Halazonetis
National and Kapodistrian University of Athens · GRUniversity of Geneva · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Genomic instability is a characteristic of most cancers. In hereditary cancers, genomic instability results from mutations in DNA repair genes and drives cancer development, as predicted by the mutator hypothesis. In sporadic (non-hereditary) cancers the molecular basis of genomic instability remains unclear, but recent high-throughput sequencing studies suggest that mutations in DNA repair genes are infrequent before therapy, arguing against the mutator hypothesis for these cancers. Instead, the mutation patterns of the tumour suppressor TP53 (which encodes p53), ataxia telangiectasia mutated (ATM) and cyclin-dependent kinase inhibitor 2A (CDKN2A; which encodes p16INK4A and p14ARF) support the oncogene-induced DNA replication stress model, which attributes genomic instability and TP53 and ATM mutations to oncogene-induced DNA damage.

Indexed as

Genomic InstabilityMutationAnimalsAtaxia Telangiectasia Mutated ProteinsCell Cycle ProteinsCyclin-Dependent Kinase Inhibitor p16DNA-Binding ProteinsDNA DamageHumansModels, BiologicalNeoplasmsProtein Serine-Threonine KinasesTumor Suppressor Protein p53Tumor Suppressor ProteinsAtaxia Telangiectasia Mutated ProteinsATM protein, humanCell Cycle ProteinsCyclin-Dependent Kinase Inhibitor p16DNA-Binding ProteinsProtein Serine-Threonine KinasesTumor Suppressor Protein p53Tumor Suppressor Proteins

Identifiers

PMID20177397
OpenAlexW1538419182

What OpenQuestion holds

Textmetadata
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.