Evidence map›Paper›PMID 21192095›Full record

ReviewGlia2011

Glutamate and the biology of gliomas.

John de Groot, Harald Sontheimer

Registry-linked trialAbstract readReview
In one paragraph

Review in Glia, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05775458 (Role of Glutamate-mediate Excitotoxicity in Invasion and Progression Processes of Glioblastoma Multiforme), which is not on this map. Cited by 166 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
166citing papers in PubMed, 1 pooled it
6.0field-weighted citation impact, top 2% 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.

NCT05775458 recruitingnot on this mapstarted 2020, after this paper: background citation

Role of Glutamate-mediate Excitotoxicity in Invasion and Progression Processes of Glioblastoma Multiforme

TypeobservationalSponsorIRCCS San RaffaeleRan2020 to 2029Enrolled50ConditionsBrain Tumor, PrimaryArmsBlood, CSF and tumor samples
3 · Its place in the literature

Who cites it

166 citing papers in PubMed, 1 synthesis or guideline pooled it, 294 citations in OpenAlex.

  1. Pooled it
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  6. Inhibitory glutamatergic feedback for brain tumor therapy.Medical oncology (Northwood, London, England) · 2026
    Review
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106 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

2 authors at 2 institutions in 1 country.

John de GrootDepartment of Neuro-Oncology, The University of Texas M.D. Anderson Cancer Center, Houston, Texas, USA.
Harald Sontheimer
The University of Texas MD Anderson Cancer Center · USUniversity of Alabama at Birmingham · US

Funding

Amino Acid Transport and the Biology of Human GliomasR01NS052634 · NINDS · VIRGINIA POLYTECHNIC INST AND ST UNIV · PI SONTHEIMER, HARALD W · 2005 to 2015
$3.7M
NINDS NIH HHS R01 NS052634NINDS NIH HHS R01-NS052634
6 · The paper itself

Abstract

Several important and previously unrecognized roles for the neurotransmitter glutamate in the biology of primary brain tumors have recently been elucidated. Glutamate is produced and released from glioma cells via the system x(c) (-) cystine glutamate transporter as a byproduct of glutathione synthesis. Glutamate appears to play a central role in the malignant phenotype of glioma via multiple mechanisms. By binding to peritumoral neuronal glutamate receptors, glutamate is responsible for seizure induction and similarly causes excitotoxicity, which aids the expansion of tumor cells into the space vacated by destroyed tissue. Glutamate also activates ionotropic and metabotropic glutamate receptors on glioma cells in a paracrine and autocrine manner. α-Amino-3-hydroxy-5-methyl-4-isoaxazolepropionate acid (AMPA) glutamate receptors lack the GluR2 subunit rendering them Ca(2+) permeable and capable of activating the AKT and MAPK pathways. Furthermore, these receptors are critical in aiding the invasion of glioma cells into normal brain. AMPA-Rs accumulate at focal adhesion sites where they may indirectly mediate interactions between the extracellular matrix and integrins. Glutamate receptor stimulation results in activation of focal adhesion kinase, which is critical to the regulation of growth factor and integrin-stimulated cell motility and invasion. The multitude of effects of glutamate on glioma biology supports the rationale for pharmacological targeting of glutamate receptors and transporters. Several ongoing and recently completed clinical trials are exploring the therapeutic potential of interrupting glutamate-mediated brain tumor growth.

Indexed as

AnimalsBenzodiazepinesBrainBrain NeoplasmsGliomaGlutamic AcidHumansModels, BiologicalReceptors, AMPASignal TransductionBenzodiazepinesglutamate receptor ionotropic, AMPA 2Glutamic AcidReceptors, AMPAtalampanel

Identifiers

PMID21192095
PMCPMC3107875
OpenAlexW2120453252

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

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.