Evidence map›Paper›PMID 37686522›Full record

ArticleCancers2023

The Impact of ETV6-NTRK3 Oncogenic Gene Fusions on Molecular and Signaling Pathway Alterations.

Matias Kinnunen, Xiaonan Liu, Elina Niemelä, Tiina Öhman, Lisa Gawriyski, Kari Salokas, Salla Keskitalo, Markku Varjosalo

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
3.7field-weighted citation impact, top 6% 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

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.

  1. A Systematic Review with a Demonstrative Case of KIT and DOG-1 Expressing Gastrointestinal Stromal Tumors Harboring ETV6-NTRK3 Fusions.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025
    Pooled it
  2. Article
  3. Article
  4. Article
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  6. Article
  7. ETV6::NTRK3-associated papillary adenocarcinoma: let us play it by ear.Virchows Archiv : an international journal of pathology · 2024
    Article
  8. Review
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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

8 authors at 1 institution in 1 country.

Matias KinnunenInstitute of Biotechnology, University of Helsinki, 00014 Helsinki, Finland.
Xiaonan LiuInstitute of Biotechnology, University of Helsinki, 00014 Helsinki, Finland.ORCID 0000-0002-9600-0536
Elina NiemeläInstitute of Biotechnology, University of Helsinki, 00014 Helsinki, Finland.ORCID 0000-0001-6871-6441
Tiina ÖhmanInstitute of Biotechnology, University of Helsinki, 00014 Helsinki, Finland.ORCID 0000-0001-6647-8873
Lisa GawriyskiInstitute of Biotechnology, University of Helsinki, 00014 Helsinki, Finland.ORCID 0000-0002-1950-4749
Kari SalokasInstitute of Biotechnology, University of Helsinki, 00014 Helsinki, Finland.ORCID 0000-0002-4471-6698
Salla KeskitaloInstitute of Biotechnology, University of Helsinki, 00014 Helsinki, Finland.
Markku VarjosaloInstitute of Biotechnology, University of Helsinki, 00014 Helsinki, Finland.ORCID 0000-0002-1340-9732
University of Helsinki · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chromosomal translocations creating fusion genes are common cancer drivers. The oncogenic ETV6-NTRK3 (EN) gene fusion joins the sterile alpha domain of the ETV6 transcription factor with the tyrosine kinase domain of the neurotrophin-3 receptor NTRK3. Four EN variants with alternating break points have since been detected in a wide range of human cancers. To provide molecular level insight into EN oncogenesis, we employed a proximity labeling mass spectrometry approach to define the molecular context of the fusions. We identify in total 237 high-confidence interactors, which link EN fusions to several key signaling pathways, including ERBB, insulin and JAK/STAT. We then assessed the effects of EN variants on these pathways, and showed that the pan NTRK inhibitor Selitrectinib (LOXO-195) inhibits the oncogenic activity of EN2, the most common variant. This systems-level analysis defines the molecular framework in which EN oncofusions operate to promote cancer and provides some mechanisms for therapeutics.

Indexed as

BioIDbiotin proximity labelingbreakpoint variantETV6-NTRK3gene fusioninteraction analysismass spectrometryproteomics

Identifiers

PMID37686522
PMCPMC10486691
OpenAlexW4386141834

What OpenQuestion 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 OpenQuestion graph.