Evidence map›Paper›PMID 11607824›Full record

ReviewOncogene2001

Biology of EWS/ETS fusions in Ewing's family tumors.

A Arvand, C T Denny

Abstract readReview
PubMed Publisher
In one paragraph

Review in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 130 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
130citing papers in PubMed, 1 pooled it
14.1field-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

130 citing papers in PubMed, 1 synthesis or guideline pooled it, 345 citations in OpenAlex.

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  6. International journal of molecular sciences · 2024
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  20. Distinct roles of hnRNPH1 low-complexity domains in splicing and transcription.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article

70 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

2 authors at 2 institutions in 1 country.

A ArvandDepartment of Pathology and Laboratory Medicine, Gwynne Hazen Cherry Memorial Labs, University of California at Los Angeles, California, USA.
C T Denny
University of California, Los Angeles · USWhite Memorial Medical Center · US

Funding

PHS HHS R01-87771
6 · The paper itself

Abstract

Tumor-associated chromosomal translocations lead to the formation of chimeric fusions between the EWS gene and one of five different ETS transcription factors in Ewing's family tumors (EFTs). The resultant EWS/ETS proteins promote oncogenesis in a dominant fashion in model systems and are necessary for continued growth of EFT cell lines. EWS belongs to a family of genes that encode proteins that may serve as adapters between the RNA polymerase II complex and RNA splicing factors. EWS/ETS fusions have biochemical characteristics of aberrant transcription factors and appear to promote abnormal cellular growth by transcriptionally modulating a network of target genes. Early evidence suggests that EWS/ETS proteins may also impact gene expression through alteration in RNA processing. Elucidation of EWS/ETS target gene networks in the context of other signaling pathways will hopefully lead to biology based therapeutic strategies for EFT.

Indexed as

Cell DivisionHeterogeneous-Nuclear RibonucleoproteinsKaryotypingModels, BiologicalModels, GeneticMultigene FamilyNeoplasmsOncogene Proteins, FusionProtein BindingProtein Structure, TertiaryRibonucleoproteinsRNARNA-Binding Protein EWSSarcoma, EwingTranslocation, GeneticHeterogeneous-Nuclear RibonucleoproteinsOncogene Proteins, FusionRibonucleoproteinsRNARNA-Binding Protein EWS

Identifiers

PMID11607824
OpenAlexW2049762189

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.