Evidence map›Paper›PMID 23085431›Full record

ReviewPharmacology & therapeutics2013

Prospects and challenges for the development of new therapies for Ewing sarcoma.

Patrick J Grohar, Lee J Helman

Open access · greenAbstract readReview
In one paragraph

Review in Pharmacology & therapeutics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
4.4field-weighted citation impact, top 6% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.

  1. Pooled it
  2. 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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  6. Review
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  13. Establishment of a novel patient-derived Ewing's sarcoma cell line, NCC-ES1-C1.In vitro cellular & developmental biology. Animal · 2018
    Article
  14. Matrix Screen Identifies Synergistic Combination of PARP Inhibitors and Nicotinamide Phosphoribosyltransferase (NAMPT) Inhibitors in Ewing Sarcoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2017
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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

2 authors at 2 institutions in 1 country.

Patrick J GroharDepartment of Pediatrics, Vanderbilt University School of Medicine and the Monroe Carrell Junior Children's Hospital, Vanderbilt-Ingram Cancer Center, 2220 Pierce Ave, PRB 397, Nashville, TN 37232-6310, USA. patrick.grohar@vanderbilt.edu
Lee J Helman
Monroe Carell Jr. Children's Hospital · USNational Cancer Institute · US

Funding

Molecular Biology of Pediatric TumorsZIASC006892 · NCI · DIVISION OF CLINICAL SCIENCES - NCI · PI HELMAN, LEE J. · 2009 to 2017
$6.3M
Solid TumorsZIASC006891 · NCI · DIVISION OF CLINICAL SCIENCES - NCI · PI HELMAN, LEE J. · 2009 to 2017
$5.0M
Solid Tumors30Z01SC006891 · SC · DIVISION OF CLINICAL SCIENCES - NCI · PI HELMAN, LEE J. · 1996 to 2008
$1.4M
Intramural NIH HHS Z01 SC006891Intramural NIH HHS ZIA SC006891
6 · The paper itself

Abstract

The Ewing sarcoma family of tumors or Ewing sarcoma (ES) is the second most common malignant bone tumor of childhood. The prognosis for localized Ewing sarcoma has improved through the development of intense multimodal therapy over the past several decades. Unfortunately, patients with recurrent or metastatic disease continue to have a poor prognosis. Therefore, a number of complementary approaches are being developed in both the preclinical and clinical arenas to improve these outcomes. In this review, we will discuss efforts to directly target the biologic drivers of this disease and relate these efforts to the experience with several different agents both in the clinic and under development. We will review the data for compounds that have shown excellent activity in the clinic, such as the camptothecins, and summarize the biological data that supports this activity. In addition, we will review the clinical experience with IGF1 targeted agents, ET-743 and epigenetically targeted therapies, the substantial amount of literature that supports their activity in Ewing sarcoma and the challenges remaining translating these therapies to the clinic. Finally, we will highlight recent work aimed at directly targeting the EWS-FLI1 transcription factor with small molecules in Ewing tumors.

Indexed as

Molecular Targeted TherapyAntineoplastic AgentsBone NeoplasmsCamptothecinClinical Trials as TopicDioxolesEpigenesis, GeneticHumansPoly(ADP-ribose) Polymerase InhibitorsSarcoma, EwingSomatomedinsTetrahydroisoquinolinesTrabectedinAntineoplastic AgentsCamptothecinDioxolesPoly(ADP-ribose) Polymerase InhibitorsSomatomedinsTetrahydroisoquinolinesTrabectedin

Identifiers

PMID23085431
PMCPMC7243921
OpenAlexW1973353533

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.