Evidence map›Paper›PMID 27577084›Full record

ArticleOncotarget2016

Efficacy of ATR inhibitors as single agents in Ewing sarcoma.

Maria Nieto-Soler, Isabel Morgado-Palacin, Vanesa Lafarga, Emilio Lecona, Matilde Murga, Elsa Callen, Daniel Azorin, Javier Alonso, Andres J Lopez-Contreras, Andre Nussenzweig and 1 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

58 citing papers in PubMed, 83 citations in OpenAlex.

  1. Targeted and molecular therapies in Ewing sarcoma: a comprehensive review of preclinical and clinical advances.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
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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

11 authors at 7 institutions in 4 countries.

Maria Nieto-SolerGenomic Instability Group, Spanish National Cancer Research Centre (CNIO), Madrid, Spain.
Isabel Morgado-PalacinGenomic Instability Group, Spanish National Cancer Research Centre (CNIO), Madrid, Spain.
Vanesa LafargaGenomic Instability Group, Spanish National Cancer Research Centre (CNIO), Madrid, Spain.
Emilio LeconaGenomic Instability Group, Spanish National Cancer Research Centre (CNIO), Madrid, Spain.
Matilde MurgaGenomic Instability Group, Spanish National Cancer Research Centre (CNIO), Madrid, Spain.
Elsa CallenLaboratory of Genome Integrity, National Cancer Institute, NIH, Bethesda, Maryland, USA.
Daniel AzorinDepartment of Pathology, Hospital Universitario Niño Jesus, Madrid, Spain.
Javier AlonsoPediatric Solid Tumor Laboratory, Institute of Rare Disease Research, ISCIII, Madrid, Spain.
Andres J Lopez-ContrerasCenter for Chromosome Stability, Department of Cellular and Molecular Medicine, Panum Institute, University of Copenhagen, Denmark.
Andre NussenzweigLaboratory of Genome Integrity, National Cancer Institute, NIH, Bethesda, Maryland, USA.
Oscar Fernandez-CapetilloGenomic Instability Group, Spanish National Cancer Research Centre (CNIO), Madrid, Spain.
Spanish National Cancer Research Centre · ESHospital Infantil Universitario Niño Jesús · ESInstituto de Salud Carlos III · ESNational Cancer Institute · USNational Human Genome Research Institute · USScience for Life Laboratory · SEUniversity of Copenhagen · DK

Funding

DNA RepairZIABC010283 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI NUSSENZWEIG, ANDRE A. · 2009 to 2025
$27.0M
European Research Council 617840
6 · The paper itself

Abstract

Ewing sarcomas (ES) are pediatric bone tumors that arise from a driver translocation, most frequently EWS/FLI1. Current ES treatment involves DNA damaging agents, yet the basis for the sensitivity to these therapies remains unknown. Oncogene-induced replication stress (RS) is a known source of endogenous DNA damage in cancer, which is suppressed by ATR and CHK1 kinases. We here show that ES suffer from high endogenous levels of RS, rendering them particularly dependent on the ATR pathway. Accordingly, two independent ATR inhibitors show in vitro toxicity in ES cell lines as well as in vivo efficacy in ES xenografts as single agents. Expression of EWS/FLI1 or EWS/ERG oncogenic translocations sensitizes non-ES cells to ATR inhibitors. Our data shed light onto the sensitivity of ES to genotoxic agents, and identify ATR inhibitors as a potential therapy for Ewing Sarcomas.

Indexed as

AnimalsAntineoplastic AgentsApoptosisAtaxia Telangiectasia Mutated ProteinsBone NeoplasmsCell Line, TumorDNA DamageGene Expression Regulation, NeoplasticHumansMaleMiceMice, SCIDRNA-Binding Protein EWSRNA, Small InterferingSarcoma, EwingSignal TransductionAntineoplastic AgentsAtaxia Telangiectasia Mutated ProteinsATR protein, humanRNA-Binding Protein EWSRNA, Small InterferingATRcancerDNA repairEwing sarcomareplication stress

Identifiers

PMID27577084
PMCPMC5312273
OpenAlexW2513016538

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.