ReviewFrontiers in oncology2026
Beyond synapses non-synaptic neural microenvironment interactions remodel circuits and drive glioma progression.
Review in Frontiers in oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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0 citing papers in PubMed.
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Authors and funding
7 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Genomic and epigenomic alterations alone cannot fully account for glioma infiltration, therapeutic resistance, or symptom severity. This review proposes a shift toward viewing the neural microenvironment as an active driver of glioma progression through diverse non-synaptic mechanisms, including metabolic coupling, ionic and volume transmission, gap junction signaling, and tumor microtube connectivity. We systematically map the contributions of astrocytes, oligodendrocyte precursor cell programs, microglia/macrophages, and the neurovascular unit, highlighting how their interactions contribute to local excitation-inhibition imbalances and disruptions in large-scale neural connectivity. These circuit-level disturbances closely correspond with clinically significant manifestations such as glioma-related epilepsy, cognitive deficits, and mood disorders, and also demonstrate correlations with patient survival outcomes. To rigorously connect molecular mechanisms to observable circuit disruptions, we integrate advanced methodologies including single-cell and spatial multi-omics analyses, human brain organoids and organotypic slice models,
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