ReviewAdvanced biology2022
Neuron-Glial Interactions in Health and Brain Cancer.
Review in Advanced biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed, 32 citations in OpenAlex.
- Oncohistone inhibition reshapes tumor-microenvironment communication in Diffuse Midline Glioma (DMG).bioRxiv : the preprint server for biology · 2026Article
- High-Throughput Discovery of Near-Infrared Oxazine Probes for Fluorescence-Guided Glioblastoma Surgery.Cancers · 2026Article
- SRSF1 as a promising biomarker and key player in the pathogenesis of Alzheimer's disease.Molecular medicine reports · 2026Article
- Neuro-glioma activity-dependent growth mechanisms: an actionable circuit from NLGN3-ADAM10 to AMPA synapses.Translational cancer research · 2026Review
- Consensus statement on microglial and macrophage functions in gliomas.Acta neuropathologica · 2026Review
- Astrocytes in neuroinflammation and brain cancer.Molecular biomedicine · 2026Review
- Pro-tumoral CaScientific reports · 2026Article
- The influence of neuro-tumor interactions on tumorigenesis and therapeutic response.Experimental hematology & oncology · 2026Review
- Beyond synapses non-synaptic neural microenvironment interactions remodel circuits and drive glioma progression.Frontiers in oncology · 2026Review
- The glioma neuron symbiosis hypothesis-cellular and molecular mechanistic considerations.Frontiers in neuroscience · 2026Article
- Neuron-Glioma Synapses in Tumor Progression.Biomedicines · 2025Review
- Diversity, Functional Complexity, and Translational Potential of Glial Cells in the Central Nervous System.International journal of molecular sciences · 2025Review
- Review
- The Many Lives of an Oligodendrocyte Precursor Cell.Annual review of neuroscience · 2025Review
- Dissecting the immune landscape in pediatric high-grade glioma reveals cell state changes under therapeutic pressure.Cell reports. Medicine · 2025Article
- Gene regulatory networks analysis for the discovery of prognostic genes in gliomas.Scientific reports · 2025Article
- The Complexity of Malignant Glioma Treatment.Cancers · 2025Review
- Invasion and metastasis in cancer: molecular insights and therapeutic targets.Signal transduction and targeted therapy · 2025Review
- Integrating priorities at the intersection of cancer and neuroscience.Cancer cell · 2025Article
- Glioma neuron symbiosis: a hypothesis.Frontiers in neuroscience · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Brain tumors are devastating diseases of the central nervous system. Brain tumor pathogenesis depends on both tumor-intrinsic oncogenic programs and extrinsic microenvironmental factors, including neurons and glial cells. Glial cells (oligodendrocytes, astrocytes, and microglia) make up half of the cells in the brain, and interact with neurons to modulate neurodevelopment and plasticity. Many brain tumor cells exhibit transcriptomic profiles similar to macroglial cells (oligodendrocytes and astrocytes) and their progenitors, making them likely to subvert existing neuron-glial interactions to support tumor pathogenesis. For example, oligodendrocyte precursor cells, a putative glioma cell of origin, can form bona fide synapses with neurons. Such synapses are recently identified in gliomas and drive glioma pathophysiology, underscoring how brain tumor cells can take advantage of neuron-glial interactions to support cancer progression. In this review, it is briefly summarized how neurons and their activity normally interact with glial cells and glial progenitors, and it is discussed how brain tumor cells utilize neuron-glial interactions to support tumor initiation and progression. Unresolved questions on these topics and potential avenues to therapeutically target neuron-glia-cancer interactions in the brain are also pointed out.
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.