Evidence map›Paper›PMID 30353492›Full record

ArticleMolecular neurobiology2019

Extracellular Vesicles Released by Glioblastoma Cells Stimulate Normal Astrocytes to Acquire a Tumor-Supportive Phenotype Via p53 and MYC Signaling Pathways.

S Hallal, D M Mallawaaratchy, H Wei, S Ebrahimkhani, B W Stringer, B W Day, A W Boyd, G J Guillemin, M E Buckland, Kimberley L Kaufman

Open access · hybridAbstract read
In one paragraph

Article in Molecular neurobiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed, 1 pooled it
4.3field-weighted citation impact, top 5% 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

84 citing papers in PubMed, 1 synthesis or guideline pooled it, 119 citations in OpenAlex.

  1. Pooled it
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  18. Intrinsic and Microenvironmental Drivers of Glioblastoma Invasion.International journal of molecular sciences · 2024
    Review
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24 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

10 authors at 3 institutions in 2 countries.

S HallalBrainstorm Brain Cancer Research, Brain and Mind Centre, University of Sydney, Level 7, 94 Mallett St, Camperdown, NSW, 2050, Australia.
D M MallawaaratchyBrainstorm Brain Cancer Research, Brain and Mind Centre, University of Sydney, Level 7, 94 Mallett St, Camperdown, NSW, 2050, Australia.
H WeiBrainstorm Brain Cancer Research, Brain and Mind Centre, University of Sydney, Level 7, 94 Mallett St, Camperdown, NSW, 2050, Australia.
S EbrahimkhaniBrainstorm Brain Cancer Research, Brain and Mind Centre, University of Sydney, Level 7, 94 Mallett St, Camperdown, NSW, 2050, Australia.
B W StringerBrain Cancer Research Unit, QIMR Berghofer Medical Research Institute, Brisbane, QLD, Australia.
B W DayBrain Cancer Research Unit, QIMR Berghofer Medical Research Institute, Brisbane, QLD, Australia.
A W BoydBrain Cancer Research Unit, QIMR Berghofer Medical Research Institute, Brisbane, QLD, Australia.
G J GuilleminDepartment of Biomedical Sciences, Faculty of Medicine and Health Sciences, Macquarie University, Sydney, NSW, Australia.
M E BucklandBrainstorm Brain Cancer Research, Brain and Mind Centre, University of Sydney, Level 7, 94 Mallett St, Camperdown, NSW, 2050, Australia.
Kimberley L KaufmanBrainstorm Brain Cancer Research, Brain and Mind Centre, University of Sydney, Level 7, 94 Mallett St, Camperdown, NSW, 2050, Australia. kim.kaufman@sydney.edu.au.ORCID http://orcid.org/0000-0002-7239-039X
The University of Sydney · AUQIMR Berghofer Medical Research Institute · AUMacquarie University · AU

Funding

Australian Rotary Health Postgraduate AwardCancer Institute NSW (AU) 13/ECF/1-17National Health and Medical Research Council 632970
6 · The paper itself

Abstract

The role of astrocytes is becoming increasingly important to understanding how glioblastoma (GBM) tumor cells diffusely invade the brain. Yet, little is known of the contribution of extracellular vesicle (EV) signaling in GBM/astrocyte interactions. We modeled GBM-EV signaling to normal astrocytes in vitro to assess whether this mode of intercellular communication could support GBM progression. EVs were isolated and characterized from three patient-derived GBM stem cells (NES

Indexed as

Signal TransductionAgedAstrocytesBrain NeoplasmsCell DifferentiationCell Line, TumorCellular SenescenceExtracellular VesiclesGelatinGlioblastomaHumansMaleMiddle AgedNanoparticlesNeoplastic Stem CellsParticle SizeGelatinProtein IsoformsProteomeProto-Oncogene Proteins c-mycTumor Suppressor Protein p53AstrocytesExtracellular vesiclesGlioblastoma stem-like cellsMYCPodosome formationSenescence-associated secretory phenotypeTP53

Identifiers

PMID30353492
PMCPMC6505517
OpenAlexW2897787848

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.