Evidence map›Paper›PMID 15806161›Full record

ArticleOncogene2005

Somatic heterozygous mutations in ETV6 (TEL) and frequent absence of ETV6 protein in acute myeloid leukemia.

Sahar Barjesteh van Waalwijk van Doorn-Khosrovani, Dominik Spensberger, Yvonne de Knegt, Michelle Tang, Bob Löwenberg, Ruud Delwel

Abstract read
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In one paragraph

Article in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

40 citing papers in PubMed, 73 citations in OpenAlex.

  1. ETV6 mutations in early immature human T cell leukemias.The Journal of experimental medicine · 2011
    Trial
  2. Article
  3. A germlineScience advances · 2025
    Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Identification of key long non-coding RNAs in gastric adenocarcinoma.Cancer biomarkers : section A of Disease markers · 2020
    Article
  13. Case reports in hematology · 2020
    Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Review
  20. Deregulation of the protein phosphatase 2A, PP2A in cancer: complexity and therapeutic options.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Review
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

6 authors at 2 institutions in 1 country.

Sahar Barjesteh van Waalwijk van Doorn-KhosrovaniDepartment of Hematology, ErasmusMC, Dr Molewaterplein 50, Rotterdam 3015GE, The Netherlands.
Dominik Spensberger
Yvonne de Knegt
Michelle Tang
Bob Löwenberg
Ruud Delwel
Erasmus MC · NLErasmus University Rotterdam · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

ETV6 (ets translocation variant gene 6) TEL (translocation ets leukemia), encoding a transcriptional repressor, is involved in various translocations associated with human malignancies. Strikingly, the nonrearranged ETV6 allele is often deleted or inactivated in cells harboring these translocations. Although ETV6 translocations are infrequent in acute myeloid leukemia (AML), mutations or deregulated expression of ETV6 may contribute to leukemogenesis. To investigate the involvement of ETV6 in AML, we analysed 300 newly diagnosed patients for mutations in the coding region of the gene. Furthermore, we studied protein expression in 77 patients using two ETV6-specific antibodies. Five somatic heterozygous mutations were detected, which affected either the homodimerization- or the DNA-binding domain of ETV6. The proteins translated from the cDNAs of these mutants were unable to repress transcription and showed dominant-negative effects. In addition, we demonstrate that one-third of AML patients have deficient ETV6 protein expression, which is not related to ETV6 mRNA expression levels. In conclusion, we demonstrate that ETV6 abnormalities are not restricted to translocations and occur more frequently in AML than previously thought. Additional comprehensive studies are required to define the clinical consequence of ETV6 loss of function in AML.

Indexed as

Gene DeletionHeterozygoteMutationTranslocation, GeneticAcute DiseaseBone Marrow CellsDNA-Binding ProteinsETS Translocation Variant 6 ProteinGene FrequencyHumansLeukemia, MyeloidNuclear ProteinsPhosphoproteinsProto-Oncogene Proteins c-etsRepressor ProteinsSequence DeletionDNA-Binding ProteinsETS Translocation Variant 6 ProteinNuclear ProteinsPhosphoproteinsProto-Oncogene Proteins c-etsRepressor Proteins

Identifiers

PMID15806161
OpenAlexW2156013165

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.