Evidence map›Paper›PMID 7623854›Full record

ArticleMolecular and cellular biology1995

Identification of target genes for the Ewing's sarcoma EWS/FLI fusion protein by representational difference analysis.

B S Braun, R Frieden, S L Lessnick, W A May, C T Denny

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
13.0field-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

58 citing papers in PubMed, 165 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Fusion transcripts: Unexploited vulnerabilities in cancer?Wiley interdisciplinary reviews. RNA · 2020
    Review
  7. Article
  8. Role for the EWS domain of EWS/FLI in binding GGAA-microsatellites required for Ewing sarcoma anchorage independent growth.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  9. Article
  10. Article
  11. Article
  12. Oncogenic fusion protein EWS-FLI1 is a network hub that regulates alternative splicing.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
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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

5 authors at 2 institutions in 1 country.

B S BraunMolecular Biology Institute, University of California, Los Angeles 90024, USA.
R Frieden
S L Lessnick
W A May
C T Denny
University of California, Los Angeles · USSidney Kimmel Comprehensive Cancer Center · US

Funding

UCLA-Caltech Medical Scientist Training ProgramT32GM008042 · NIGMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI AJIJOLA, OLUJIMI A, DAWSON, DAVID WAYNE · 1985 to 2023
$29.9M
NIGMS NIH HHS GM08042
6 · The paper itself

Abstract

The EWS/FLI-1 fusion gene results from the 11;22 chromosomal translocation in Ewing's sarcoma. The product of the gene is one of a growing number of structurally altered transcription factors implicated in oncogenesis. We have employed a subtractive cloning strategy of representational difference analysis in conjunction with a model transformation system to identify genes transcribed in response to EWS/FLI. We have characterized eight transcripts that are dependent on EWS/FLI for expression and two transcripts that are repressed in response to EWS/FLI. Three of the former were identified by sequence analysis as stromelysin 1, a murine homolog of cytochrome P-450 F1 and cytokeratin 15. Stromelysin 1 is induced rapidly after expression of EWS/FLI, suggesting that the stromelysin 1 gene may be a direct target gene of EWS/FLI. These results demonstrate that expression of EWS/FLI leads to significant changes in the transcription of specific genes and that these effects are at least partially distinct from those caused by expression of germ line FLI-1. The representational difference analysis technique can potentially be applied to investigate transformation pathways activated by a broad array of genes in different tumor systems.

Indexed as

Proto-Oncogene ProteinsBase SequenceDNA-Binding ProteinsDNA, ComplementaryGene Expression Regulation, NeoplasticHeterogeneous-Nuclear RibonucleoproteinsMatrix Metalloproteinase 3MetalloendopeptidasesMolecular BiologyMolecular Sequence DataNeoplasm ProteinsNuclear ProteinsProto-Oncogene Protein c-fli-1RibonucleoproteinsRNA-Binding Protein EWSRNA-Binding ProteinsDNA-Binding ProteinsDNA, ComplementaryHeterogeneous-Nuclear RibonucleoproteinsMatrix Metalloproteinase 3MetalloendopeptidasesNeoplasm ProteinsNuclear ProteinsProto-Oncogene Protein c-fli-1Proto-Oncogene ProteinsRibonucleoproteinsRNA-Binding Protein EWSRNA-Binding ProteinsRNA, MessengerRNA, NeoplasmTrans-Activators

Identifiers

PMID7623854
PMCPMC230703
OpenAlexW2147598399

What Socratic 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 Socratic graph.