Evidence map›Paper›PMID 23935076›Full record

ArticleNucleic acids research2013

Systems biology of Ewing sarcoma: a network model of EWS-FLI1 effect on proliferation and apoptosis.

Gautier Stoll, Didier Surdez, Franck Tirode, Karine Laud, Emmanuel Barillot, Andrei Zinovyev, Olivier Delattre

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

31 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
  2. Genetically Engineered Mouse Model in Ewing Sarcoma.Methods in molecular biology (Clifton, N.J.) · 2027
    Article
  3. Article
  4. Article
  5. Genomic alterations and diagnosis of renal cancer.Virchows Archiv : an international journal of pathology · 2024
    Review
  6. Review
  7. Article
  8. Article
  9. Systems Biology Analysis for Ewing Sarcoma.Methods in molecular biology (Clifton, N.J.) · 2021
    Article
  10. Article
  11. Review: Ewing Sarcoma Predisposition.Pathology oncology research : POR · 2020
    Review
  12. Precision medicine in Ewing sarcoma: a translational point of view.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2020
    Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. GEFT aberrant expression in soft tissue sarcomas.Translational cancer research · 2019
    Article
  19. Article
  20. Article
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.

Gautier StollInstitut Curie, 26 rue d'Ulm, 75248 Paris cedex 05, France, INSERM U900, Bioinformatique, biostatistique et épidémiologie d'un système complexe, Paris, France, Mines ParisTech, Fontainebleau, France, INSERM U830, Unité de Génétique et Biologie des Cancers, Paris, France and Institut Curie, Unité de génétique somatique, Paris, France.
Didier Surdez
Franck Tirode
Karine Laud
Emmanuel Barillot
Andrei Zinovyev
Olivier Delattre
Inserm · FRInstitut Curie · FRÉcole Nationale Supérieure des Mines de Paris · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ewing sarcoma is the second most frequent pediatric bone tumor. In most of the patients, a chromosomal translocation leads to the expression of the EWS-FLI1 chimeric transcription factor that is the major oncogene in this pathology. Relative genetic simplicity of Ewing sarcoma makes it particularly attractive for studying cancer in a systemic manner. Silencing EWS-FLI1 induces cell cycle alteration and ultimately leads to apoptosis, but the exact molecular mechanisms underlying this phenotype are unclear. In this study, a network linking EWS-FLI1 to cell cycle and apoptosis phenotypes was constructed through an original method of network reconstruction. Transcriptome time-series after EWS-FLI1 silencing were used to identify core modulated genes by an original scoring method based on fitting expression profile dynamics curves. Literature data mining was then used to connect these modulated genes into a network. The validity of a subpart of this network was assessed by siRNA/RT-QPCR experiments on four additional Ewing cell lines and confirmed most of the links. Based on the network and the transcriptome data, CUL1 was identified as a new potential target of EWS-FLI1. Altogether, using an original methodology of data integration, we provide the first version of EWS-FLI1 network model of cell cycle and apoptosis regulation.

Indexed as

Cell ProliferationGene Regulatory NetworksApoptosisBone NeoplasmsCell Line, TumorData MiningGene Expression Regulation, NeoplasticHumansModels, GeneticOncogene Proteins, FusionProto-Oncogene Protein c-fli-1RNA-Binding Protein EWSRNA, Small InterferingSarcoma, EwingSignal TransductionSystems BiologyEWS-FLI fusion proteinOncogene Proteins, FusionProto-Oncogene Protein c-fli-1RNA-Binding Protein EWSRNA, Small Interfering

Identifiers

PMID23935076
PMCPMC3799442
OpenAlexW2048524108

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.