Evidence map›Paper›PMID 36915128›Full record

ArticleActa neuropathologica communications2023

Immunological and tumor-intrinsic mechanisms mediate the synergistic growth suppression of experimental glioblastoma by radiotherapy and MET inhibition.

Manuela Silginer, Eleanna Papa, Emese Szabó, Flavio Vasella, Martin Pruschy, Christopher Stroh, Patrick Roth, Tobias Weiss, Michael Weller

Open access · goldFull text read
PubMed Full text at PMC Publisher
In one paragraph

Article in Acta neuropathologica communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

4 citing papers in PubMed, 4 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
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

9 authors at 3 institutions in 2 countries.

Manuela SilginerLaboratory of Molecular Neuro-Oncology, Department of Neurology, University Hospital of Zurich, Frauenklinikstrasse 26, 8091, Zurich, Switzerland. manuela.silginer@usz.ch.ORCID 0000-0003-2538-1244
Eleanna PapaLaboratory of Molecular Neuro-Oncology, Department of Neurology, University of Zurich, Zurich, Switzerland.
Emese SzabóLaboratory of Molecular Neuro-Oncology, Department of Neurology, University of Zurich, Zurich, Switzerland.
Flavio VasellaLaboratory of Molecular Neuro-Oncology, Department of Neurology, University Hospital of Zurich, Frauenklinikstrasse 26, 8091, Zurich, Switzerland.
Martin PruschyLaboratory for Molecular Radiobiology, Department of Radiation Oncology, University Hospital and University of Zurich, Zurich, Switzerland.
Christopher StrohMerck Healthcare KGaA, Darmstadt, Germany.
Patrick RothLaboratory of Molecular Neuro-Oncology, Department of Neurology, University Hospital of Zurich, Frauenklinikstrasse 26, 8091, Zurich, Switzerland.
Tobias WeissLaboratory of Molecular Neuro-Oncology, Department of Neurology, University Hospital of Zurich, Frauenklinikstrasse 26, 8091, Zurich, Switzerland.
Michael WellerLaboratory of Molecular Neuro-Oncology, Department of Neurology, University Hospital of Zurich, Frauenklinikstrasse 26, 8091, Zurich, Switzerland.
University of Zurich · CHUniversity Hospital of Zurich · CHMerck (Germany) · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The hepatocyte growth factor (HGF)/MET signaling pathway has been proposed to be involved in the resistance to radiotherapy of glioblastoma via proinvasive and DNA damage response pathways.Here we assessed the role of the MET pathway in the response to radiotherapy in vitro and in vivo in syngeneic mouse glioma models. We find that the murine glioma cell lines GL-261, SMA-497, SMA-540 and SMA-560 express HGF and its receptor MET and respond to exogenous HGF with MET phosphorylation. Glioma cell viability or proliferation are unaffected by genetic or pharmacological MET inhibition using tepotinib or CRISPR/Cas9-engineered Met gene knockout and MET inhibition fails to sensitize glioma cells to irradiation in vitro. In contrast, the combination of tepotinib with radiotherapy prolongs survival of orthotopic SMA-560 or GL-261 glioma-bearing mice compared with radiotherapy or tepotinib treatment alone. Synergy is lost when such experiments are conducted in immunodeficient Rag1

Indexed as

Brain NeoplasmsGlioblastomaGliomaAnimalsCell Line, TumorMicePhosphorylationSignal TransductionGliomaHGFImmunotherapyIrradiationSynergy

Identifiers

PMID36915128
PMCPMC10009975
OpenAlexW4324089276

What OpenQuestion holds

Textfull text, public
LicenceCC BY
measurements read43
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.