Evidence map›Paper›PMID 24746645›Full record

ReviewDNA repair2014

DNA double-strand break repair pathway choice and cancer.

Tomas Aparicio, Richard Baer, Jean Gautier

Abstract readReview
In one paragraph

Review in DNA repair, 2014. 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
11.2field-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

197 citing papers in PubMed, 1 synthesis or guideline pooled it, 349 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. GSK3βGut · 2026
    Article
  4. Review
  5. Article
  6. Article
  7. DNA damage and repair in cardiomyopathy: mechanisms and therapeutic opportunities.American journal of physiology. Heart and circulatory physiology · 2026
    Review
  8. Review
  9. Article
  10. Article
  11. NovelFrontiers in endocrinology · 2026
    Article
  12. Review
  13. DNA Damage and Repair in Pancreatic Cancer-The Latest Findings.International journal of molecular sciences · 2025
    Review
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Review
  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

3 authors at 2 institutions in 1 country.

Tomas AparicioInstitute for Cancer Genetics & Department of Genetics and Development, Columbia University Medical Center, New York, NY, USA.
Richard BaerInstitute for Cancer Genetics & Department of Pathology and Cell Biology, Columbia University Medical Center, New York, NY, USA.
Jean GautierInstitute for Cancer Genetics & Department of Genetics and Development, Columbia University Medical Center, New York, NY, USA. Electronic address: jg130@columbia.edu.
Cancer Genetics (United States) · USColumbia University Irving Medical Center · US

Funding

The Role of CTIP in Lymphocyte Development and LymphomagenesisP01CA174653 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI RABADAN, RAUL · 2014 to 2024
$17.6M
Regulation of the DNA damage response by the MRN-ATM pathwayR01CA092245 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI GAUTIER, JEAN · 2002 to 2015
$4.0M
Studies of DNA interstrand crosslink repair to improve crosslinking drug therapieR01CA167826 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI GAUTIER, JEAN · 2012 to 2015
$1.3M
NCI NIH HHS P01 CA174653NCI NIH HHS R01 CA092245NCI NIH HHS R01 CA167826
6 · The paper itself

Abstract

Since DNA double-strand breaks (DSBs) contribute to the genomic instability that drives cancer development, DSB repair pathways serve as important mechanisms for tumor suppression. Thus, genetic lesions, such as BRCA1 and BRCA2 mutations, that disrupt DSB repair are often associated with cancer susceptibility. In addition, recent evidence suggests that DSB "mis-repair", in which DSBs are resolved by an inappropriate repair pathway, can also promote genomic instability and presumably tumorigenesis. This notion has gained currency from recent cancer genome sequencing studies which have uncovered numerous chromosomal rearrangements harboring pathological DNA repair signatures. In this perspective, we discuss the factors that regulate DSB repair pathway choice and their consequences for genome stability and cancer.

Indexed as

DNA Breaks, Double-StrandedBRCA1 ProteinCarcinogenesisDNA End-Joining RepairDNA RepairGenomic InstabilityHumansIntracellular Signaling Peptides and ProteinsNeoplasmsRecombination, GeneticSignal TransductionTumor Suppressor p53-Binding Protein 1BRCA1 ProteinBRCA1 protein, humanIntracellular Signaling Peptides and ProteinsTP53BP1 protein, humanTumor Suppressor p53-Binding Protein 153BP1–BRCA1DNA double strand breakDNA endsMicrohomology-mediated end joiningRepair pathway choiceResection

Identifiers

PMID24746645
PMCPMC4051845
OpenAlexW2090854519

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.