Evidence map›Paper›PMID 27748748›Full record

ArticleNature medicine2016

Recurrent MET fusion genes represent a drug target in pediatric glioblastoma.

International Cancer Genome Consortium PedBrain Tumor Project

Open access · greenAbstract read
PubMed Publisher
In one paragraph

Article in Nature medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 134 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
134citing papers in PubMed, 1 pooled it
16.1field-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

134 citing papers in PubMed, 1 synthesis or guideline pooled it, 239 citations in OpenAlex.

  1. Pooled it
  2. Vebreltinib for Previously Treated Astrocytoma,Cancer communications (London, England) · 2026
    Trial
  3. Phase II Trial of Dabrafenib Plus Trametinib in Relapsed/RefractoryJournal of clinical oncology : official journal of the American Society of Clinical Oncology · 2023
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74 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

1 author at 20 institutions in 11 countries.

International Cancer Genome Consortium PedBrain Tumor Project
German Cancer Research Center · DEHeidelberg University · DEUniversity Hospital Heidelberg · DEEuropean Molecular Biology Laboratory · DEMax Planck Institute for Molecular Genetics · DEUniversity of Freiburg · DECentre National de la Recherche Scientifique · FRGerman Marine Research Consortium · DEHeinrich Heine University Düsseldorf · DEHôpital Farhat Hached · TNInstitute of Cancer Research · GBMcGill University · CANational Center for Tumor Diseases · DENew York University · USNYU Langone Health · USThe University of Western Australia · AUBurdenko Neurosurgery Institute · RUCharles University · CZChinese University of Hong Kong · HKDeutschen Konsortium für Translationale Krebsforschung · DE

Funding

Vaccine FacilityP30CA016087 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI ADRIANA HEGUY · 1985 to 2026
$83.1M
Institutional Clinical and Translational Science AwardUL1TR000038 · NCATS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI CRONSTEIN, BRUCE NEIL · 2012 to 2014
$16.8M
Cancer Research UK 11736Cancer Research UK 13982NCATS NIH HHS UL1 TR000038NCI NIH HHS P30 CA016087
6 · The paper itself

Abstract

Pediatric glioblastoma is one of the most common and most deadly brain tumors in childhood. Using an integrative genetic analysis of 53 pediatric glioblastomas and five in vitro model systems, we identified previously unidentified gene fusions involving the MET oncogene in ∼10% of cases. These MET fusions activated mitogen-activated protein kinase (MAPK) signaling and, in cooperation with lesions compromising cell cycle regulation, induced aggressive glial tumors in vivo. MET inhibitors suppressed MET tumor growth in xenograft models. Finally, we treated a pediatric patient bearing a MET-fusion-expressing glioblastoma with the targeted inhibitor crizotinib. This therapy led to substantial tumor shrinkage and associated relief of symptoms, but new treatment-resistant lesions appeared, indicating that combination therapies are likely necessary to achieve a durable clinical response.

Indexed as

AdolescentAdultAnilidesAnimalsBrain NeoplasmsCell Line, TumorChildChild, PreschoolCrizotinibDNA, NeoplasmFemaleGlioblastomaHumansInfantMaleMiceAnilidesCrizotinibcytoplasmic linker protein 115DNA, NeoplasmGSK 1363089Microtubule-Associated ProteinsMitogen-Activated Protein KinasesOncogene Proteins, FusionProtein Kinase InhibitorsProteinsProto-Oncogene Proteins c-metPTPRZ1 protein, humanPyrazolesPyridinesQuinolinesReceptor-Like Protein Tyrosine Phosphatases, Class 5RNA, MessengerTFG protein, humanVesicular Transport Proteins

Identifiers

PMID27748748
OpenAlexW2533448509

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.