Evidence map›Paper›PMID 20547696›Full record

ReviewClinical cancer research : an official journal of the American Association for Cancer Research2010

Oncogenic partnerships: EWS-FLI1 protein interactions initiate key pathways of Ewing's sarcoma.

Hayriye V Erkizan, Vladimir N Uversky, Jeffrey A Toretsky

Open access · bronzeAbstract readReview
In one paragraph

Review in Clinical cancer research : an official journal of the American Association for Cancer Research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed
10.4field-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

83 citing papers in PubMed, 157 citations in OpenAlex.

  1. Trial
  2. Open-Label, Multicenter, Phase I/II, First-in-Human Trial of TK216: A First-Generation EWS::FLI1 Fusion Protein Antagonist in Ewing Sarcoma.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2024
    Trial
  3. Trial
  4. Review
  5. Article
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  8. Article
  9. Article
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  12. Targeted degradation of α-Synuclein using an evolved botulinum toxin protease.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  13. Review
  14. Review
  15. Unlocking epigenetics for precision treatment of Ewing's sarcoma.Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2024
    Article
  16. Article
  17. Article
  18. Review
  19. Article
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23 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

3 authors at 3 institutions in 2 countries.

Hayriye V ErkizanDepartment of Oncology and Pediatrics, Lombardi Comprehensive Cancer Center, Georgetown University, Washington, DC, USA.
Vladimir N Uversky
Jeffrey A Toretsky
Georgetown University · USIndiana University – Purdue University Indianapolis · USInstitute for Biological Instrumentation · RU

Funding

YK-4-279 specifically targets ETS family fusion-protein cancers in clinical trialRC4CA156509 · NCI · GEORGETOWN UNIVERSITY · PI TORETSKY, JEFFREY A · 2010 to 2010
$4.4M
Isolation and small molecule targeting of Ewing's Sarcoma stem cellsR01CA138212 · NCI · GEORGETOWN UNIVERSITY · PI TORETSKY, JEFFREY A · 2008 to 2012
$2.4M
Novel Compounds to Inactivate Oncogenic Fusion ProteinsR01CA133662 · NCI · GEORGETOWN UNIVERSITY · PI TORETSKY, JEFFREY A · 2009 to 2013
$1.5M
NCI NIH HHS R01 CA133662NCI NIH HHS R01 CA138212NCI NIH HHS RC4 CA156509
6 · The paper itself

Abstract

Targeted therapy for cancer, which is specifically directed toward the cancer without any potential for effects outside of controlling the tumor, is a gold standard for treatment. Ewing's sarcoma contains the potential target EWS-FLI1, as a result of a pathognomonic chromosomal translocation. The EWS-FLI1 fusion protein includes the EWS domain, a potent transcriptional activator alongside the highly conserved FLI1 ets DNA-binding domain. Because of the combination of these domains, the EWS-FLI1 fusion protein acts as an aberrant transcription factor whose expression results in cellular transformation. EWS-FLI1 functions by binding to normal cellular protein partners in transcription and splicing, similar to how a virus would corrupt normal cellular machinery for virion production. Therefore, understanding the protein-protein interactions of EWS-FLI1 and the pathways that are regulated by these partnerships will inform both oncogenesis and therapeutics. This review describes the known protein partners and transcriptional targets of EWS-FLI1, while proposing strategies for exploiting these partnerships with targeted therapy.

Indexed as

AnimalsGene Expression Regulation, NeoplasticHumansOncogene Proteins, FusionProto-Oncogene Protein c-fli-1RNA-Binding Protein EWSSarcoma, EwingSignal TransductionTranscription FactorsTranscription, GeneticTranslocation, GeneticEWS-FLI fusion proteinOncogene Proteins, FusionProto-Oncogene Protein c-fli-1RNA-Binding Protein EWSTranscription Factors

Identifiers

PMID20547696
PMCPMC3682924
OpenAlexW2122260140

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.