Evidence map›Paper›PMID 36505823›Full record

ReviewFrontiers in oncology2022

The importance of fusion protein activity in Ewing sarcoma and the cell intrinsic and extrinsic factors that regulate it: A review.

April A Apfelbaum, Emma D Wrenn, Elizabeth R Lawlor

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
5.9field-weighted citation impact, top 3% 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

29 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  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
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Review
  16. Review
  17. Article
  18. 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

3 authors at 2 institutions in 1 country.

April A ApfelbaumBen Towne Center for Childhood Cancer Research, Seattle Children's Research Institute and Department of Pediatrics, University of Washington, Seattle, WA, United States.
Emma D WrennBen Towne Center for Childhood Cancer Research, Seattle Children's Research Institute and Department of Pediatrics, University of Washington, Seattle, WA, United States.
Elizabeth R LawlorBen Towne Center for Childhood Cancer Research, Seattle Children's Research Institute and Department of Pediatrics, University of Washington, Seattle, WA, United States.
University of Washington · USSeattle Children's Hospital · US

Funding

Regulation and function of HOX genes in Ewing sarcoma pathogenesisR01CA215981 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LAWLOR, ELIZABETH R · 2018 to 2022
$2.0M
The role of HOXD13 in controlling Ewing sarcoma cell plasticity and metastasisF31CA247104 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI APFELBAUM, APRIL · 2021 to 2022
$66k
NCI NIH HHS F31 CA247104NCI NIH HHS R01 CA215981
6 · The paper itself

Abstract

Accumulating evidence shows that despite clonal origins tumors eventually become complex communities comprised of phenotypically distinct cell subpopulations. This heterogeneity arises from both tumor cell intrinsic programs and signals from spatially and temporally dynamic microenvironments. While pediatric cancers usually lack the mutational burden of adult cancers, they still exhibit high levels of cellular heterogeneity that are largely mediated by epigenetic mechanisms. Ewing sarcomas are aggressive bone and soft tissue malignancies with peak incidence in adolescence and the prognosis for patients with relapsed and metastatic disease is dismal. Ewing sarcomas are driven by a single pathognomonic fusion between a FET protein and an ETS family transcription factor, the most common of which is EWS::FLI1. Despite sharing a single driver mutation, Ewing sarcoma cells demonstrate a high degree of transcriptional heterogeneity both between and within tumors. Recent studies have identified differential fusion protein activity as a key source of this heterogeneity which leads to profoundly different cellular phenotypes. Paradoxically, increased invasive and metastatic potential is associated with

Indexed as

cell phenotypeEwing sarcomaheterogeneityoncogeneplasticity

Identifiers

PMID36505823
PMCPMC9727305
OpenAlexW4309716480

What Socratic 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 Socratic graph.