Evidence map›Paper›PMID 27170701›Full record

ReviewJournal of radiation research2016

Unsolved mystery: the role of BRCA1 in DNA end-joining.

Janapriya Saha, Anthony J Davis

Abstract readReview
In one paragraph

Review in Journal of radiation research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
–field-weighted citation impact
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

22 citing papers in PubMed.

  1. International journal of molecular sciences · 2026
    Review
  2. Article
  3. Complex Interplay Between Obesity and BRCA1/2-Associated Breast Cancer: An Overview.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2025
    Review
  4. Review
  5. Article
  6. CTLA-4 Facilitates DNA Damage-Induced Apoptosis by Interacting With PP2A.Frontiers in cell and developmental biology · 2022
    Article
  7. Article
  8. The repair geneOncology reviews · 2021
    Article
  9. Single-Strand Annealing in Cancer.International journal of molecular sciences · 2021
    Review
  10. Review
  11. Review
  12. Article
  13. Review
  14. Review
  15. Review
  16. Article
  17. Can Designer Indels Be Tailored by Gene Editing?: Can Indels Be Customized?BioEssays : news and reviews in molecular, cellular and developmental biology · 2019
    Article
  18. Article
  19. Article
  20. Review
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.

Janapriya SahaDepartment of Radiation Oncology, Division of Molecular Radiation Biology, University of Texas Southwestern Medical Center, 2201 Inwood Rd, Dallas, Texas 75390-9187, USA.
Anthony J DavisDepartment of Radiation Oncology, Division of Molecular Radiation Biology, University of Texas Southwestern Medical Center, 2201 Inwood Rd, Dallas, Texas 75390-9187, USA anthony.davis@utsouthwestern.edu.

Funding

Transcription-Coupled & Replication-Associated Excision RepairP01CA092584 · NCI · UNIVERSITY OF CALIF-LAWRENC BERKELEY LAB · PI John A. Tainer · 2001 to 2026
$89.6M
Pathway Choice of DNA Double-Strand Break RepairR01CA162804 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI DAVIS, ANTHONY J · 2012 to 2021
$3.4M
NCI NIH HHS P01 CA092584NCI NIH HHS R01 CA162804
6 · The paper itself

Abstract

Heritable mutations in the tumor suppressor gene BRCA1 increase a woman's lifetime risk of developing breast and ovarian cancer. BRCA1's tumor suppressor function is directly linked to its myriad of functions in the cellular response to DNA double-strand breaks (DSBs). BRCA1 interacts with an extensive array of DNA damage responsive proteins and plays important roles in DSB repair, mediated by the homologous recombination pathway, and in the activation of cell cycle checkpoints. However, the role of BRCA1 in the other two DSB repair pathways, classical non-homologous end-joining (C-NHEJ) and alternative NHEJ (A-NHEJ), remains unclear. In this review, we will discuss the current literature on BRCA1's potential role(s) in modulating both C-NHEJ and A-NHEJ. We also present a model showing that BRCA1 contributes to genomic maintenance by promoting precise DNA repair across all cell cycle phases via the direct modulation of DNA end-joining.

Indexed as

DNA End-Joining RepairAnimalsBRCA1 ProteinBreast NeoplasmsCell CycleDNA Breaks, Double-StrandedFemaleHumansModels, BiologicalBRCA1 ProteinBRCA1breast cancerDNA-PKcsHRKu70/80NHEJ

Identifiers

PMID27170701
PMCPMC4990114

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.