ReviewInternational journal of molecular sciences2023
The Role of Hyperexcitability in Gliomagenesis.
Review in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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.
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
21 citing papers in PubMed.
- Neuro-glioma activity-dependent growth mechanisms: an actionable circuit from NLGN3-ADAM10 to AMPA synapses.Translational cancer research · 2026Review
- The influence of neuro-tumor interactions on tumorigenesis and therapeutic response.Experimental hematology & oncology · 2026Review
- Cancer Neuroscience: Linking Neuronal Plasticity with Brain Tumor Growth and Resistance.Biology · 2026Review
- Neuron-Glioma Synapses in Tumor Progression.Biomedicines · 2025Review
- Connectomics in brain tumor surgery: large-scale clinical feasibility and hypothesis-generating tractometry findings.Journal of neuro-oncology · 2025Article
- Alcohol use disorder and epileptogenesis in primary malignant brain tumors: temporal and tumor grade associations in a nationwide EHR cohort study.medRxiv : the preprint server for health sciences · 2025Article
- Pan-cancer neural regulation pattern with implications for patient stratification and immunotherapy.Molecular therapy. Nucleic acids · 2025Article
- Therapeutic approaches for targeting the pediatric brain tumor microenvironment.Drug delivery and translational research · 2025Review
- Hydroxytyrosol and Brain Tumors: Mechanisms of Action and Therapeutic Potential.Current issues in molecular biology · 2025Review
- Presurgical structural connectivity predicts postsurgical cognitive impairment in glioma patients.Brain communications · 2025Article
- Tumor-related epilepsy in high-grade glioma: a large series survival analysis.Journal of neuro-oncology · 2024Article
- Multi-omics Analysis Revealed that the CCN Family Regulates Cell Crosstalk, Extracellular Matrix, and Immune Escape, Leading to a Poor Prognosis of Glioma.Cell biochemistry and biophysics · 2024Article
- Gliomagenesis, Epileptogenesis, and Remodeling of Neural Circuits: Relevance for Novel Treatment Strategies in Low- and High-Grade Gliomas.International journal of molecular sciences · 2024Review
- The immune system and metabolic products in epilepsy and glioma-associated epilepsy: emerging therapeutic directions.JCI insight · 2024Review
- Review
- Multiscale network neuroscience in neuro-oncology: How tumors, brain networks, and behavior connect across scales.Neuro-oncology practice · 2023Review
- Ion Channels and Ionotropic Receptors in Astrocytes: Physiological Functions and Alterations in Alzheimer's Disease and Glioblastoma.Life (Basel, Switzerland) · 2023Review
- Differential metabolic alterations in IDH1 mutant vs. wildtype glioma cells promote epileptogenesis through distinctive mechanisms.Frontiers in cellular neuroscience · 2023Review
- Hippocampal ΔFosB expression is associated with cognitive impairment in a subgroup of patients with childhood epilepsies.Frontiers in neurology · 2023Article
- Seizure outcomes as an understudied metric in glioma clinical trials: A review of the ClinicalTrials.gov database.Neuro-oncology advancesReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma is the most common malignant primary brain tumor. Recent studies have demonstrated that excitatory or activity-dependent signaling-both synaptic and non-synaptic-contribute to the progression of glioblastoma. Glutamatergic receptors may be stimulated via neuron-tumor synapses or release of glutamate by the tumor itself. Ion currents generated by these receptors directly alter the structure of membrane adhesion molecules and cytoskeletal proteins to promote migratory behavior. Additionally, the hyperexcitable milieu surrounding glioma increases the rate at which tumor cells proliferate and drive recurrent disease. Inhibition of excitatory signaling has shown to effectively reduce its pro-migratory and -proliferative effects.
Indexed as
Identifiers
What OpenQuestion holds
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.