Evidence map›Paper›PMID 17875932›Full record

ArticleMolecular and cellular biology2007

EWS/FLI-1 induces rapid onset of myeloid/erythroid leukemia in mice.

Enrique C Torchia, Kelli Boyd, Jerold E Rehg, Chunxu Qu, Suzanne J Baker

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

60 citing papers in PubMed, 91 citations in OpenAlex.

  1. Trial
  2. A Drosophila Study Model for EWS::FLI1-Induced Molecular Pathways.Methods in molecular biology (Clifton, N.J.) · 2027
    Article
  3. Article
  4. Acute Erythroid Leukemia: From Molecular Biology to Clinical Outcomes.International journal of molecular sciences · 2024
    Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. CDKs in Sarcoma: Mediators of Disease and Emerging Therapeutic Targets.International journal of molecular sciences · 2020
    Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Translocations involving ETS family proteins in human cancer.Integrative cancer science and therapeutics · 2018
    Article
  16. Article
  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

5 authors at 2 institutions in 2 countries.

Enrique C TorchiaDepartment of Developmental Neurobiology, Hartwell Center, St. Jude Children's Research Hospital, 332 N. Lauderdale St., Memphis, Tennessee 38105, USA.
Kelli Boyd
Jerold E Rehg
Chunxu Qu
Suzanne J Baker
St. Jude Children's Research Hospital · USGenetic Resources Center · JP

Funding

Molecular Pathogenesis of Ewing SarcomaR01CA092117 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI BAKER, SUZANNE J · 2001 to 2005
$1.2M
NCI NIH HHS CA92117NCI NIH HHS R01 CA092117
6 · The paper itself

Abstract

EWS/FLI-1 is a chimeric oncogene generated by chromosomal translocation in Ewing tumors, a family of poorly differentiated pediatric tumors arising predominantly in bone but also in soft tissue. The fusion gene combines sequences encoding a strong transactivating domain from the EWS protein with the DNA binding domain of FLI-1, an ETS transcription factor. A related fusion, TLS/ERG, has been found in myeloid leukemia. To determine EWS/FLI-1 function in vivo, we engineered mice with Cre-inducible expression of EWS/FLI-1 from the ubiquitous Rosa26 locus. When crossed with Mx1-cre mice, Cre-mediated activation of EWS/FLI-1 resulted in the rapid development of myeloid/erythroid leukemia characterized by expansion of primitive mononuclear cells causing hepatomegaly, splenomegaly, severe anemia, and death. The disease could be transplanted serially into naïve recipients. Gene expression profiles of primary and transplanted animals were highly similar, suggesting that activation of EWS/FLI-1 was the primary event leading to disease in this model. The Cre-inducible EWS/FLI-1 mouse provides a novel model system to study the contribution of this oncogene to malignant disease in vivo.

Indexed as

Mice, TransgenicStem CellsAnimalsCell LineCell ProliferationChimeraChromosome AberrationsGATA1 Transcription FactorGene Expression ProfilingLeukemia, MyeloidMiceMice, Inbred C57BLMice, Inbred NODMice, SCIDNeoplasm TransplantationOncogene Proteins, FusionEWS-FLI fusion proteinGata1 protein, mouseGATA1 Transcription FactorGt(ROSA)26Sor non-coding RNA, mouseOncogene Proteins, FusionProteinsProto-Oncogene Protein c-fli-1RNA-Binding Protein EWSRNA, Untranslated

Identifiers

PMID17875932
PMCPMC2169157
OpenAlexW2127975227

What OpenQuestion holds

Textmetadata
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.