Evidence map›Paper›PMID 28659469›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2017

ATM loss leads to synthetic lethality in BRCA1 BRCT mutant mice associated with exacerbated defects in homology-directed repair.

Chun-Chin Chen, Elizabeth M Kass, Wei-Feng Yen, Thomas Ludwig, Mary Ellen Moynahan, Jayanta Chaudhuri, Maria Jasin

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
3.1field-weighted citation impact, top 7% 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

40 citing papers in PubMed, 63 citations in OpenAlex.

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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

7 authors at 3 institutions in 1 country.

Chun-Chin ChenDevelopmental Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065.
Elizabeth M KassDevelopmental Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065.
Wei-Feng YenBiochemistry & Structural Biology, Cell & Developmental Biology, and Molecular Biology (BCMB) Allied Program, Weill Cornell Graduate School of Medical Sciences, Cornell University, New York, NY 10065.
Thomas LudwigDepartment of Cancer Biology and Genetics, Ohio State University College of Medicine, Columbus, OH 43210.
Mary Ellen MoynahanDepartment of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY 10065.
Jayanta ChaudhuriImmunology Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065.
Maria JasinDevelopmental Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065; m-jasin@ski.mskcc.org.
Memorial Sloan Kettering Cancer Center · USCornell University · USThe Ohio State University · US

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Nicholas D Socci · 1985 to 2026
$347.4M
The Role of Id Proteins in Breast TumorigenesisP01CA094060 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI LOWE, SCOTT W. · 2002 to 2018
$39.4M
Training and Career Development and Education CoreU54CA137788 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI Daniel Alan Heller · 2008 to 2026
$28.1M
Mechanistic Elucidation of Class Switch Recombination and Somatic HypermutationR01AI072194 · NIAID · SLOAN-KETTERING INST CAN RESEARCH · PI CHAUDHURI, JAYANTA · 2009 to 2025
$6.9M
RNA-directed targeting of AID in immunity and genomic integrityR01AI124186 · NIAID · SLOAN-KETTERING INST CAN RESEARCH · PI Jayanta Chaudhuri · 2016 to 2026
$4.8M
HOMOLOGY-DIRECTED DNA REPAIR PROTEINS BRCA2 AND RAD51 PARALOGS IN TUMOR-RELEVANT TISSUESR01CA185660 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI JASIN, MARIA · 2014 to 2020
$2.7M
Homologous recombination mechanisms in mammalian cellsR35GM118175 · NIGMS · SLOAN-KETTERING INST CAN RESEARCH · PI JASIN, MARIA · 2016 to 2020
$2.6M
Double-Strand Break Repair in Mouse Mammary Gland Development and TumorigenesisK99CA184122 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI KASS, ELIZABETH · 2014 to 2015
$284k
NCI NIH HHS K99 CA184122NCI NIH HHS P01 CA094060NCI NIH HHS P30 CA008748NCI NIH HHS R01 CA185660NCI NIH HHS U54 CA137788NIAID NIH HHS R01 AI072194NIAID NIH HHS R01 AI124186NIGMS NIH HHS R35 GM118175
6 · The paper itself

Abstract

BRCA1 is essential for homology-directed repair (HDR) of DNA double-strand breaks in part through antagonism of the nonhomologous end-joining factor 53BP1. The ATM kinase is involved in various aspects of DNA damage signaling and repair, but how ATM participates in HDR and genetically interacts with BRCA1 in this process is unclear. To investigate this question, we used the

Indexed as

DNA RepairSynthetic Lethal MutationsAnimalsAtaxia Telangiectasia Mutated ProteinsBRCA1 ProteinDNA Breaks, Double-StrandedDNA End-Joining RepairEmbryonic Stem CellsEpistasis, GeneticFibroblastsGene DeletionGreen Fluorescent ProteinsHomologous RecombinationMiceMice, Mutant StrainsMutationAtaxia Telangiectasia Mutated ProteinsAtm protein, mouseBRCA1 ProteinBrca1 protein, mouseGreen Fluorescent ProteinsolaparibPhthalazinesPiperazinesTrp53bp1 protein, mouseTumor Suppressor p53-Binding Protein 1Tumor Suppressor ProteinsATMBRCA1homologous recombinationhomology-directed repairolaparib

Identifiers

PMID28659469
PMCPMC5530697
OpenAlexW2728023387

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.