Evidence map›Paper›PMID 26873923›Full record

ArticleNucleic acids research2016

Targeting BRCA1- and BRCA2-deficient cells with RAD52 small molecule inhibitors.

Fei Huang, Nadish Goyal, Katherine Sullivan, Kritika Hanamshet, Mikir Patel, Olga M Mazina, Charles X Wang, W Frank An, James Spoonamore, Shailesh Metkar and 4 more

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed
5.9field-weighted citation impact, top 3% 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

76 citing papers in PubMed, 96 citations in OpenAlex.

  1. Article
  2. Article
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  4. Targeting RAD52 overcomes PARP inhibitor resistance in preclinicalbioRxiv : the preprint server for biology · 2025
    Article
  5. Article
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  9. Transcriptomics and Proteomics Analysis of the Liver ofInternational journal of molecular sciences · 2025
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16 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

14 authors at 4 institutions in 1 country.

Fei HuangDepartment of Biochemistry and Molecular Biology, Drexel University College of Medicine, Philadelphia, PA 19102, USA.
Nadish GoyalDepartment of Biochemistry and Molecular Biology, Drexel University College of Medicine, Philadelphia, PA 19102, USA.
Katherine SullivanDepartment of Microbiology and Immunology, and Fels Institute for Cancer Research and Molecular Biology, Temple University School of Medicine, Philadelphia, PA 10140, USA.
Kritika HanamshetDepartment of Biochemistry and Molecular Biology, Drexel University College of Medicine, Philadelphia, PA 19102, USA.
Mikir PatelDepartment of Biochemistry and Molecular Biology, Drexel University College of Medicine, Philadelphia, PA 19102, USA.
Olga M MazinaDepartment of Biochemistry and Molecular Biology, Drexel University College of Medicine, Philadelphia, PA 19102, USA.
Charles X WangDepartment of Biochemistry and Molecular Biology, Drexel University College of Medicine, Philadelphia, PA 19102, USA.
W Frank AnBroad Institute of Harvard and Massachusetts Institute of Technology, Cambridge, MA 02142, USA.
James SpoonamoreBroad Institute of Harvard and Massachusetts Institute of Technology, Cambridge, MA 02142, USA.
Shailesh MetkarBroad Institute of Harvard and Massachusetts Institute of Technology, Cambridge, MA 02142, USA.
Kyle A EmmitteVanderbilt Specialized Chemistry Center for Accelerated Probe Development, Vanderbilt Center for Neuroscience Drug Discovery, Department of Pharmacology and Chemistry, Vanderbilt University, Nashville, TN 37232, USA.
Simon CocklinDepartment of Biochemistry and Molecular Biology, Drexel University College of Medicine, Philadelphia, PA 19102, USA.
Tomasz SkorskiDepartment of Microbiology and Immunology, and Fels Institute for Cancer Research and Molecular Biology, Temple University School of Medicine, Philadelphia, PA 10140, USA.
Alexander V MazinDepartment of Biochemistry and Molecular Biology, Drexel University College of Medicine, Philadelphia, PA 19102, USA Alexander.Mazin@DrexelMed.edu.
Drexel University · USMassachusetts Institute of Technology · USTemple University · USVanderbilt University · US

Funding

WORD PROCESSING CENTER--COREP30CA006927 · NCI · RESEARCH INST OF FOX CHASE CAN CTR · PI Margaret von Mehren · 1985 to 2026
$138.8M
User Driven ProjectU54HG005032 · NHGRI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI SCHREIBER, STUART L · 2008 to 2013
$88.1M
The Vanderbilt Specialized Chemistry Center for Accelerated Probe DevelopmentU54MH084659 · NIMH · VANDERBILT UNIVERSITY · PI LINDSLEY, CRAIG · 2008 to 2013
$24.1M
Targeting DNA repair to eradicate TKi-refractory/resistant CML and Ph+ALLR01CA186238 · NCI · TEMPLE UNIV OF THE COMMONWEALTH · PI SKORSKI, TOMASZ · 2014 to 2024
$4.5M
Repair of DNA breaks in human: the role of Rad54 proteinR01CA100839 · NCI · DREXEL UNIVERSITY · PI MAZIN, ALEXANDER V · 2003 to 2013
$2.6M
Small Molecule inhibitors as a new approach to study human RAD51 recombinaseR01CA188347 · NCI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI MAZIN, ALEXANDER V · 2015 to 2019
$2.5M
High-throughput Computational Docking Screen for Small-molecule Inhibitors of HIVR21AI087388 · NIAID · DREXEL UNIVERSITY · PI COCKLIN, SIMON · 2010 to 2011
$422k
NCI NIH HHS P30 CA006927NCI NIH HHS R01 CA100839NCI NIH HHS R01 CA186238NCI NIH HHS R01 CA188347NHGRI NIH HHS U54 HG005032NIAID NIH HHS R21 AI087388NIMH NIH HHS U54 MH084659
6 · The paper itself

Abstract

RAD52 is a member of the homologous recombination (HR) pathway that is important for maintenance of genome integrity. While single RAD52 mutations show no significant phenotype in mammals, their combination with mutations in genes that cause hereditary breast cancer and ovarian cancer like BRCA1, BRCA2, PALB2 and RAD51C are lethal. Consequently, RAD52 may represent an important target for cancer therapy. In vitro, RAD52 has ssDNA annealing and DNA strand exchange activities. Here, to identify small molecule inhibitors of RAD52 we screened a 372,903-compound library using a fluorescence-quenching assay for ssDNA annealing activity of RAD52. The obtained 70 putative inhibitors were further characterized using biochemical and cell-based assays. As a result, we identified compounds that specifically inhibit the biochemical activities of RAD52, suppress growth of BRCA1- and BRCA2-deficient cells and inhibit RAD52-dependent single-strand annealing (SSA) in human cells. We will use these compounds for development of novel cancer therapy and as a probe to study mechanisms of DNA repair.

Indexed as

Antineoplastic AgentsBRCA1 ProteinBRCA2 ProteinCell Line, TumorCell SurvivalCisplatinDNA DamageDrug Screening Assays, AntitumorGene Knockdown TechniquesHigh-Throughput Screening AssaysHumansInhibitory Concentration 50Protein BindingRad52 DNA Repair and Recombination ProteinAntineoplastic AgentsBRCA1 ProteinBRCA1 protein, humanBRCA2 ProteinBRCA2 protein, humanCisplatinRad52 DNA Repair and Recombination ProteinRAD52 protein, human

Identifiers

PMID26873923
PMCPMC4872086
OpenAlexW2266606089

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.