ArticleNeuron2023
Glioma epileptiform activity and progression are driven by IGSF3-mediated potassium dysregulation.
Article in Neuron, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
55 citing papers in PubMed, 1 synthesis or guideline pooled it, 77 citations in OpenAlex.
- Meta-analysis of treatment-emergent seizures in glioma vaccine trials.Journal of neuro-oncology · 2026Pooled it
- Pilot Trial of Perampanel on Peritumoral Hyperexcitability in Newly Diagnosed High-grade Glioma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024Trial
- Stroke drives glioma progression through the emergence of tumor-associated astrocytes with reduced CaNature cancer · 2026Article
- Potassium-scavenging train-style nanorobots potentiate radiotherapy and reverse immunosuppression in glioblastoma.Journal of nanobiotechnology · 2026Article
- An artefact-resilient wide bandwidth bidirectional graphene neural interface.Nature communications · 2026Article
- Leveraging neuroscience imaging and electrophysiological assessments to decode neuron-glioma interactions.Neuro-oncology advances · 2026Review
- H3 dopaminylation and CaMKII modulate diffuse midline glioma response to CDK9 inhibition.bioRxiv : the preprint server for biology · 2026Article
- The influence of neuro-tumor interactions on tumorigenesis and therapeutic response.Experimental hematology & oncology · 2026Review
- Increased neural excitability and glioma synaptic activity drives glioma proliferation in human cortex.Nature neuroscience · 2026Article
- Pathological neural and immune synapses in glioblastoma progression: mechanisms and therapeutic opportunities.Frontiers in neural circuits · 2026Review
- Crosstalk in the brain tumor microenvironment: mechanisms, therapeutic strategies, and clinical advances.Military Medical Research · 2026Review
- Autonomous Microrobots for Spatiotemporally Active Therapeutic Delivery and Controlled Release.Cyborg and bionic systems (Washington, D.C.) · 2026Review
- Glioma-related epilepsy in patients with newly diagnosed and recurrent glioblastoma, IDH-wildtype: a study under the 2021 WHO CNS tumor classification.BMC cancer · 2025Article
- Aberrant neural activity in the peritumoral cortex underlies the progression of tumor-associated seizures.Nature communications · 2025Article
- State of the art: glioma-associated epilepsy-bridging tumor biology and epileptogenesis.Neurological research and practice · 2025Review
- Research progress in glioma-related epilepsy (Review).Biomedical reports · 2025Article
- Tumor-related epilepsy in glioma: A multidisciplinary overview.Epilepsia · 2025Review
- Aberrant neuronal firing: a paracrine route to glioblastoma expansion.Cell communication and signaling : CCS · 2025Article
- The excitatory milieu in glioma: Mechanisms and therapeutic avenues.Neuro-oncology · 2025Review
- Cholinergic neuronal activity promotes diffuse midline glioma growth through muscarinic signaling.Cell · 2025Article
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Authors and funding
18 authors at 3 institutions in 1 country.
Funding
Abstract
Seizures are a frequent pathophysiological feature of malignant glioma. Recent studies implicate peritumoral synaptic dysregulation as a driver of brain hyperactivity and tumor progression; however, the molecular mechanisms that govern these phenomena remain elusive. Using scRNA-seq and intraoperative patient ECoG recordings, we show that tumors from seizure patients are enriched for gene signatures regulating synapse formation. Employing a human-to-mouse in vivo functionalization pipeline to screen these genes, we identify IGSF3 as a mediator of glioma progression and dysregulated neural circuitry that manifests as spreading depolarization (SD). Mechanistically, we discover that IGSF3 interacts with Kir4.1 to suppress potassium buffering and found that seizure patients exhibit reduced expression of potassium handlers in proliferating tumor cells. In vivo imaging reveals that dysregulated synaptic activity emanates from the tumor-neuron interface, which we confirm in patients. Our studies reveal that tumor progression and seizures are enabled by ion dyshomeostasis and identify SD as a driver of disease.
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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 OpenQuestion graph.