Evidence map›Paper›PMID 32094664›Full record

ReviewNature reviews. Molecular cell biology2020

The antitumorigenic roles of BRCA1-BARD1 in DNA repair and replication.

Madalena Tarsounas, Patrick Sung

Open access · greenAbstract readReview
In one paragraph

Review in Nature reviews. Molecular cell biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 245 papers.

0numbers the graph read from it
0cells of the map it votes in
245citing papers in PubMed
17.4field-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

245 citing papers in PubMed, 354 citations in OpenAlex.

  1. Article
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  3. Review
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  5. Mechanisms and disease relevance of DNA break repair pathway choice.Nature reviews. Molecular cell biology · 2026
    Review
  6. TheBiomolecular NMR assignments · 2026
    Article
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  9. TheBiomolecular NMR assignments · 2026
    Article
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  13. International journal of molecular sciences · 2026
    Review
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  20. Article

185 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 2 institutions in 2 countries.

Madalena TarsounasGenome Stability and Tumourigenesis Group, Oxford Institute for Radiation Oncology, Department of Oncology, University of Oxford, Oxford, UK. madalena.tarsounas@oncology.ox.ac.uk.ORCID http://orcid.org/0000-0002-4273-2870
Patrick SungDepartment of Biochemistry and Structural Biology, University of Texas Health Science Center, San Antonio, TX, USA. sungp@uthscsa.edu.ORCID http://orcid.org/0000-0003-1396-9040
The University of Texas Health Science Center at San Antonio · USUniversity of Oxford · GB

Funding

YEAST DNA REPAIR GENES AND PROTEINS OF THE RAD52 GROUPR01ES007061 · NIEHS · YALE UNIVERSITY · PI Patrick Sung · 1995 to 2026
$9.4M
Mechanisms of DNA Homology-directed Genome Repair and Tumor SuppressionR35CA241801 · NCI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI SUNG, PATRICK · 2019 to 2025
$6.0M
Mechanistic Dissection of the Fanconi Anemia Pathway of DNA Damage Response and RR01CA168635 · NCI · YALE UNIVERSITY · PI Gary M Kupfer, Patrick Sung · 2013 to 2026
$5.8M
Cancer Research UK 22907Medical Research CouncilNCI NIH HHS R01 CA168635NCI NIH HHS R35 CA241801NIEHS NIH HHS R01 ES007061
6 · The paper itself

Abstract

The tumour suppressor breast cancer type 1 susceptibility protein (BRCA1) promotes DNA double-strand break (DSB) repair by homologous recombination and protects DNA replication forks from attrition. BRCA1 partners with BRCA1-associated RING domain protein 1 (BARD1) and other tumour suppressor proteins to mediate the initial nucleolytic resection of DNA lesions and the recruitment and regulation of the recombinase RAD51. The discovery of the opposing functions of BRCA1 and the p53-binding protein 1 (53BP1)-associated complex in DNA resection sheds light on how BRCA1 influences the choice of homologous recombination over non-homologous end joining and potentially other mutagenic pathways of DSB repair. Understanding the functional crosstalk between BRCA1-BARD1 and its cofactors and antagonists will illuminate the molecular basis of cancers that arise from a deficiency or misregulation of chromosome damage repair and replication fork maintenance. Such knowledge will also be valuable for understanding acquired tumour resistance to poly(ADP-ribose) polymerase (PARP) inhibitors and other therapeutics and for the development of new treatments. In this Review, we discuss recent advances in elucidating the mechanisms by which BRCA1-BARD1 functions in DNA repair, replication fork maintenance and tumour suppression, and its therapeutic relevance.

Indexed as

BRCA1 ProteinBreast NeoplasmsDNA End-Joining RepairDNA ReplicationFemaleHumansPoly(ADP-ribose) Polymerase InhibitorsPoly(ADP-ribose) PolymerasesProtein BindingRecombinational DNA RepairTumor Suppressor p53-Binding Protein 1Tumor Suppressor ProteinsUbiquitin-Protein LigasesBARD1 protein, humanBRCA1 ProteinBRCA1 protein, humanPoly(ADP-ribose) Polymerase InhibitorsPoly(ADP-ribose) PolymerasesTP53BP1 protein, humanTumor Suppressor p53-Binding Protein 1Tumor Suppressor ProteinsUbiquitin-Protein Ligases

Identifiers

PMID32094664
PMCPMC7204409
OpenAlexW3007516256

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.