ReviewBioEssays : news and reviews in molecular, cellular and developmental biology2025
What Epigenetics Teaches Us About Neuron-Glioma Interactions.
Review in BioEssays : news and reviews in molecular, cellular and developmental biology, 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.
- Neuro-glioma activity-dependent growth mechanisms: an actionable circuit from NLGN3-ADAM10 to AMPA synapses.Translational cancer research · 2026Review
- Cancer Neuroscience: Linking Neuronal Plasticity with Brain Tumor Growth and Resistance.Biology · 2026Review
- Neurobiological pathways underlying brain tumor progression: basis for oncogenicity and opportunities for immunotherapeutic intervention.Frontiers in oncology · 2026Review
- What Epigenetics Teaches Us About Neuron-Glioma Interactions.BioEssays : news and reviews in molecular, cellular and developmental biology · 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
3 authors.
Funding
Abstract
Neuron-glioma interactions are critical drivers of glioma progression, with neuronal activity promoting tumor growth and invasion through paracrine signaling and direct synaptic input. Beyond well-established glutamatergic synapses, recent discoveries revealed that GABAergic interactions also contribute to glioma proliferation. Here, we focus on how glioma cells decode neuronal cues via epigenetic mechanisms, including enhancer reprogramming, chromatin remodeling, and rewiring of 3D genome organization, with transcriptions factors such as SMAD3 and PITX1 orchestrating transcriptional programs that sustain neuron-to-glioma communication. Additionally, recent integration of multi-omics data highlights gene regulatory networks linked to GABAergic signaling as contributors to glioblastoma (GB) pathogenesis. We also underscore the distinct roles of GABAergic signaling across glioma subtypes, noting that, in GB, GABA-related metabolic and paracrine mechanisms, rather than synaptic input, may drive tumor progression. Understanding how epigenetic reprogramming facilitates glioma integration into neural circuits opens new avenues to disrupt these malignant neuron-glioma interactions by targeting the epigenetic machinery.
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.