Evidence map›Paper›PMID 31381204›Full record

ArticleBrain pathology (Zurich, Switzerland)2020

A novel PTPRZ1-ETV1 fusion in gliomas.

Alenka Matjašič, Andrej Zupan, Emanuela Boštjančič, Jože Pižem, Mara Popović, Danijela Kolenc

Open access · greenAbstract read
In one paragraph

Article in Brain pathology (Zurich, Switzerland), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.9field-weighted citation impact, top 25% 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, 14 citations in OpenAlex.

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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

6 authors at 1 institution in 1 country.

Alenka MatjašičInstitute of Pathology, Faculty of Medicine, University of Ljubljana, Ljubljana, Slovenia.ORCID 0000-0002-9933-8495
Andrej ZupanInstitute of Pathology, Faculty of Medicine, University of Ljubljana, Ljubljana, Slovenia.
Emanuela BoštjančičInstitute of Pathology, Faculty of Medicine, University of Ljubljana, Ljubljana, Slovenia.
Jože PižemInstitute of Pathology, Faculty of Medicine, University of Ljubljana, Ljubljana, Slovenia.
Mara PopovićInstitute of Pathology, Faculty of Medicine, University of Ljubljana, Ljubljana, Slovenia.ORCID 0000-0002-0443-1217
Danijela KolencInstitute of Pathology, Faculty of Medicine, University of Ljubljana, Ljubljana, Slovenia.
University of Ljubljana · SI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The aggressive nature of malignant gliomas and their genetic and clinical heterogeneity present a major challenge in their diagnosis and treatment. Development of targeted therapy brought attention on detecting novel gene fusions, since they represent promising therapeutic targets (eg, TRK inhibitors in NTRK fusion-positive tumors). Using targeted next-generation sequencing, we prospectively analyzed 205 primary brain tumors and detected a novel PTPRZ1-ETV1 fusion transcript in 11 of 191 (5.8%) gliomas, including nine glioblastomas, one anaplastic oligodendroglioma and one pilocytic astrocytoma. PTPRZ1-ETV1 fusion was confirmed by RT-PCR followed by Sanger sequencing, and in-silico analysis predicted a potential driver role. The newly detected fusion consists of the PTPRZ1 promoter in frame with the highly conserved DNA-binding domain of ETV1 transcription factor. The ETV1 and PTPRZ1 genes are known oncogenes, involved in processes of tumor development. ETV1 is a member of the ETS family of transcription factors, already known oncogenic drivers in Ewing sarcoma, prostate cancer and gastrointestinal stromal tumors, but not in gliomas. Its overexpression contributes to tumor growth and more aggressive tumor behavior. PTPRZ1 is already considered to be a tumor growth promoting oncogene in gliomas. In 8%-16% of gliomas, PTPRZ1 is fused to the MET oncogene, resulting in a PTPRZ1-MET fusion, which is associated with poorer prognosis but is also a positive predictive biomarker for treatment with kinase inhibitors. In view of the oncogenic role that the two fusion partners, PTPRZ1 and ETV1, exhibit in other malignancies, PTPRZ1-ETV1 fusion might present a novel potential therapeutic target in gliomas. Although histopathological examination of PTPRZ1-ETV1 fusion-positive gliomas did not reveal any specific or unique pathological features, and the follow-up period was too short to assess prognostic value of the fusion, careful monitoring of patients and their response to therapy might provide additional insights into the prognostic and predictive value of this novel fusion.

Indexed as

AdultAgedAged, 80 and overBrain NeoplasmsChildDNA-Binding ProteinsFemaleGliomaHumansMaleMiddle AgedOncogene FusionOncogene Proteins, FusionReceptor-Like Protein Tyrosine Phosphatases, Class 5Transcription FactorsDNA-Binding ProteinsETV1 protein, humanOncogene Proteins, FusionPTPRZ1 protein, humanReceptor-Like Protein Tyrosine Phosphatases, Class 5Transcription FactorsETV1gliomasnovel fusiononcogenesPTPRZ1RNA-sequencing

Identifiers

PMID31381204
PMCPMC8018154
OpenAlexW2966288067

What OpenQuestion holds

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Registered trials

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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.