Evidence map›Paper›PMID 38570528›Full record

ArticleNature communications2024

Mesenchymal glioma stem cells trigger vasectasia-distinct neovascularization process stimulated by extracellular vesicles carrying EGFR.

Cristiana Spinelli, Lata Adnani, Brian Meehan, Laura Montermini, Sidong Huang, Minjun Kim, Tamiko Nishimura, Sidney E Croul, Ichiro Nakano, Yasser Riazalhosseini and 1 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
6.1field-weighted citation impact, top 3% 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

20 citing papers in PubMed, 26 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

11 authors at 4 institutions in 2 countries.

Cristiana SpinelliMcGill University, The Research Institute of the McGill University Health Centre, Montreal, QC, Canada.
Lata AdnaniMcGill University, The Research Institute of the McGill University Health Centre, Montreal, QC, Canada.ORCID http://orcid.org/0000-0002-2852-6915
Brian MeehanMcGill University, The Research Institute of the McGill University Health Centre, Montreal, QC, Canada.
Laura MonterminiMcGill University, The Research Institute of the McGill University Health Centre, Montreal, QC, Canada.
Sidong HuangDepartment of Biochemistry, McGill University, Montreal, QC, Canada.ORCID http://orcid.org/0000-0002-2838-4726
Minjun KimDepartment of Human Genetics, McGill University, Montreal, QC, Canada.
Tamiko NishimuraDepartment of Human Genetics, McGill University, Montreal, QC, Canada.
Sidney E CroulDepartment of Pathology & Laboratory Medicine, Dalhousie University, Halifax, NS, Canada.
Ichiro NakanoDepartment of Neurosurgery, Hokuto Social Medical Corporation, Hokuto Hospital, Kisen-7-5 Inadacho, Obihiro, Hokkaido, 080-0833, Japan.ORCID http://orcid.org/0000-0002-0916-3207
Yasser RiazalhosseiniDepartment of Human Genetics, McGill University, Montreal, QC, Canada.ORCID http://orcid.org/0000-0003-0875-618X
Janusz RakMcGill University, The Research Institute of the McGill University Health Centre, Montreal, QC, Canada. janusz.rak@mcgill.ca.ORCID http://orcid.org/0000-0002-2912-5566
McGill University Health Centre · CAMcGill University · CADalhousie University · CAHokuto Hospital · JP

Funding

Canada Foundation for Innovation (Fondation canadienne pour l'innovation) 39799Gouvernement du Canada | Canadian Institutes of Health Research (Instituts de Recherche en Santé du Canada) PJT 183971Kidney Foundation of Canada (La Fondation canadienne du rein) N/AU.S. Department of Defense (United States Department of Defense) N/A
6 · The paper itself

Abstract

Targeting neovascularization in glioblastoma (GBM) is hampered by poor understanding of the underlying mechanisms and unclear linkages to tumour molecular landscapes. Here we report that different molecular subtypes of human glioma stem cells (GSC) trigger distinct endothelial responses involving either angiogenic or circumferential vascular growth (vasectasia). The latter process is selectively triggered by mesenchymal (but not proneural) GSCs and is mediated by a subset of extracellular vesicles (EVs) able to transfer EGFR/EGFRvIII transcript to endothelial cells. Inhibition of the expression and phosphorylation of EGFR in endothelial cells, either pharmacologically (Dacomitinib) or genetically (gene editing), abolishes their EV responses in vitro and disrupts vasectasia in vivo. Therapeutic inhibition of EGFR markedly extends anticancer effects of VEGF blockade in mice, coupled with abrogation of vasectasia and prolonged survival. Thus, vasectasia driven by intercellular transfer of oncogenic EGFR may represent a new therapeutic target in a subset of GBMs.

Indexed as

Brain NeoplasmsExtracellular VesiclesGlioblastomaGliomaAnimalsEndothelial CellsErbB ReceptorsHumansMiceNeoplastic Stem CellsEGFR protein, humanErbB Receptors

Identifiers

PMID38570528
PMCPMC10991552
OpenAlexW4393856410

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.