ReviewNeuro-oncology2025
The excitatory milieu in glioma: Mechanisms and therapeutic avenues.
Review in Neuro-oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed.
- Ivosidenib and Vorasidenib Decrease Intratumoral 2-Hydroxyglutarate and Total Choline Levels in Patients with Lower-Grade Glioma: An In Vivo MR Spectroscopy Study.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026Article
- Epilepsy characteristics and outcomes in patients with pleomorphic xanthoastrocytomas.Journal of neuro-oncology · 2026Article
- Inhibition of EIF2S1 expression regulates the PI3K/AKT pathway to mediate apoptosis in glioma cells: an in vitro study.Neurogenetics · 2026Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
Gliomas are the most common primary malignant brain tumors. Their electrobiologic properties drive disease development, and in select tumors, aberrant neurosignaling is situated at the crux of gliomagenesis and glioma-related epilepsy. Tumor microtubes and the neuronal-glioma synapse are defined components of the glioma circuitry. The nidus of cortical hyperexcitability-the peri-glioma-undergoes severe alterations during disease progression and is influenced by genetic mutations, anomalous synaptic remodeling, inflammatory changes, and an imbalance in neurotransmitters. Such pathologic mechanisms have been exploited for anticancer and anti-seizure value wherein a subset remains to be explored. In this Review, we discuss the hyperexcitable conditions within the glioma microenvironment and candidate therapies for seizure and tumor control.
Indexed as
Identifiers
What Socratic 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 Socratic graph.