ReviewPharmaceuticals (Basel, Switzerland)2025
AMPA Receptor Modulation in the Treatment of High-Grade Glioma: Translating Good Science into Better Outcomes.
Review in Pharmaceuticals (Basel, Switzerland), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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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.
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.
Who cites it
12 citing papers in PubMed.
- Review
- AMPAR Subunit Gene Expression Marks a Synaptic Transcriptional State in Lower-Grade Glioma.Brain sciences · 2026Article
- Neural regulation of cancer: from synaptic integration to neuro-immune regulation.Cellular oncology (Dordrecht, Netherlands) · 2026Review
- Metabolic Reprogramming and Neurotransmitter Signaling Co-Option in the Glioma Immune Microenvironment: Dual-Axis Regulation of Immunosuppression.Biomolecules · 2026Review
- Subgroup-Specific Associations of GRIA Genes Encoding AMPA Glutamate Receptor Subunits with Patient Survival in Medulloblastoma.Neuromolecular medicine · 2026Article
- Neuro-glioma activity-dependent growth mechanisms: an actionable circuit from NLGN3-ADAM10 to AMPA synapses.Translational cancer research · 2026Review
- Fluoxetine Acts as a Calcium-Dependent Sensitizer of TRAIL-Induced Apoptosis in Glioblastoma Multiforme.ACS omega · 2026Article
- Cancer Neuroscience: Linking Neuronal Plasticity with Brain Tumor Growth and Resistance.Biology · 2026Review
- Review of glioblastoma and systemic comorbidities.Frontiers in oncology · 2026Review
- Neuron-Glioma Synapses in Tumor Progression.Biomedicines · 2025Review
- The role of genes related to excitotoxicity in glioma prognosis.Discover oncology · 2025Article
- Glioma-neuron interactions: insights from neural plasticity.Frontiers in oncology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma (GB) treatment, despite consisting of surgical resection paired with radiation, temozolomide chemotherapy and tumor-treating fields, yields a median survival of 15-20 months. One of the more recently appreciated hallmarks of GB aggressiveness is the co-opting of neurotransmitter signaling mechanisms that normally sustain excitatory synaptic communication in the CNS. AMPA-glutamate receptor (AMPAR) signaling governs the majority of excitatory synaptic activity in the mammalian brain. AMPAR activation in glioma cells activates cellular pathways that enhance proliferation and invasion and confer resistance to approved GB therapeutics. In addition, this review places a specific emphasis on discussing the redefined GB cytoarchitecture that consists of neuron-to-glioma cell synapses, whose oncogenic activity is driven by AMPAR activation on glioma cells, and the discovery of tumor microtubes, which propagate calcium signals throughout the tumor network in order to enhance resistance to complete surgical resection and radiotherapy. These new discoveries notwithstanding, some evidence suggests that AMPAR activation can produce excitotoxicity in tumor cells. This disparity warrants a closer examination at how AMPAR modulation can be leveraged to produce more durable outcomes in the treatment of GB and tumors in peripheral organs that express AMPAR.
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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 Socratic graph.