Evidence map›Paper›PMID 20543858›Full record

ReviewOncogene2010

Recent advances in the molecular pathogenesis of Ewing's sarcoma.

E C Toomey, J D Schiffman, S L Lessnick

Open access · bronzeAbstract readReview
In one paragraph

Review in Oncogene, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 113 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
113citing papers in PubMed, 4 pooled it
15.4field-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

113 citing papers in PubMed, 4 syntheses or guidelines pooled it, 190 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Matrix metalloproteinase 2 expression and survival of patients with osteosarcoma: a meta-analysis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Pooled it
  4. Prognostic significance of p53 expression in malignant bone tumors: a meta-analysis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2013
    Pooled it
  5. Article
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  7. STAG2 loss amplifies EWS-FLI1-driven microsatellite enhancer activity promoting Ewing sarcoma aggressiveness.Proceedings of the National Academy of Sciences of the United States of America · 2026
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53 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 2 institutions in 1 country.

E C ToomeyDepartment of Oncological Sciences and Center for Children's Cancer Research, Huntsman Cancer Institute, Salt Lake City, UT 84112, USA.
J D Schiffman
S L Lessnick
Center for Children · USUniversity of Utah · US

Funding

UTAH REGIONAL CANCER CENTERP30CA042014 · NCI · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · PI Jared P Rutter · 1986 to 2026
$72.6M
EWS/FLI AND ITS TARGETS IN EWING'S SARCOMAR01CA140394 · NCI · UNIVERSITY OF UTAH · PI LESSNICK, STEPHEN L. · 2010 to 2014
$1.5M
Antibody-based detection of translocations in pediatric cancerR21CA138295 · NCI · UNIVERSITY OF UTAH · PI LESSNICK, STEPHEN L. · 2009 to 2011
$656k
NCI NIH HHS P30 CA042014NCI NIH HHS P30CA042014NCI NIH HHS R01 CA140394NCI NIH HHS R01CA140394NCI NIH HHS R21 CA138295NCI NIH HHS R21CA138295
6 · The paper itself

Abstract

Tumor development is a complex process resulting from interplay between mutations in oncogenes and tumor suppressors, host susceptibility factors, and cellular context. Great advances have been made by studying rare tumors with unique clinical, genetic, or molecular features. Ewing's sarcoma serves as an excellent paradigm for understanding tumorigenesis because it exhibits some very useful and important characteristics. For example, nearly all cases of Ewing's sarcoma contain the (11;22)(q24;q12) chromosomal translocation that encodes the EWS/FLI oncoprotein. Besides the t(11;22), however, many cases have otherwise simple karyotypes with no other demonstrable abnormalities. Furthermore, it seems that an underlying genetic susceptibility to Ewing's sarcoma, if it exists, must be rare. These two features suggest that EWS/FLI is the primary mutation that drives the development of this tumor. Finally, Ewing's sarcoma is an aggressive tumor that requires aggressive treatment. Thus, improved understanding of the pathogenesis of this tumor will not only be of academic interest, but may also lead to new therapeutic approaches for individuals afflicted with this disease. The purpose of this review is to highlight recent advances in understanding the molecular pathogenesis of Ewing's sarcoma, while considering the questions surrounding this disease that still remain and how this knowledge may be applied to developing new treatments for patients with this highly aggressive disease.

Indexed as

AnimalsCell Transformation, NeoplasticGene DosageHumansMutationRNA-Binding Protein EWSSarcoma, EwingTranscription, GeneticRNA-Binding Protein EWS

Identifiers

PMID20543858
PMCPMC3555143
OpenAlexW1996375162

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.