ArticleActa neuropathologica communications2024
Brain injury drives optic glioma formation through neuron-glia signaling.
Article in Acta neuropathologica communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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Who cites it
10 citing papers in PubMed, 8 citations in OpenAlex.
- Stroke drives glioma progression through the emergence of tumor-associated astrocytes with reduced CaNature cancer · 2026Article
- Targeting the nervous system: Mechanistic insights into neuro-tumor communication and therapeutic opportunities.Acta pharmaceutica Sinica. B · 2026Review
- CCL5 and CD11b-fibrin interactions regulate microglia migration and morphology in hyperinflammatory experimental cerebral malaria.Journal of neuroinflammation · 2026Article
- Asthma-mediated control of optic glioma growth via T cell-microglia interactions: A mathematical model.NPJ systems biology and applications · 2026Article
- Neuroscience in glioma biology (Review).Oncology reports · 2025Review
- Current states in understanding oligodendroglia-mediated neurological issues in neurofibromatosis type 1 (NF1).Acta neuropathologica communications · 2025Review
- Targeting the glioblastoma resection margin with locoregional nanotechnologies.Nature reviews. Clinical oncology · 2025Review
- Applications of Machine Learning-Driven Molecular Models for Advancing Ophthalmic Precision Medicine.Bioengineering (Basel, Switzerland) · 2025Review
- Neuropathological mRNA Expression Changes after Single Mild Traumatic Brain Injury in Pigs.Biomedicines · 2024Article
- Visual Deficits and Diagnostic and Therapeutic Strategies for Neurofibromatosis Type 1: Bridging Science and Patient-Centered Care.Vision (Basel, Switzerland) · 2024Review
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
Tissue injury and tumorigenesis share many cellular and molecular features, including immune cell (T cells, monocytes) infiltration and inflammatory factor (cytokines, chemokines) elaboration. Their common pathobiology raises the intriguing possibility that brain injury could create a tissue microenvironment permissive for tumor formation. Leveraging several murine models of the Neurofibromatosis type 1 (NF1) cancer predisposition syndrome and two experimental methods of brain injury, we demonstrate that both optic nerve crush and diffuse traumatic brain injury induce optic glioma (OPG) formation in mice harboring Nf1-deficient preneoplastic progenitors. We further elucidate the underlying molecular and cellular mechanisms, whereby glutamate released from damaged neurons stimulates IL-1β release by oligodendrocytes to induce microglia expression of Ccl5, a growth factor critical for Nf1-OPG formation. Interruption of this cellular circuit using glutamate receptor, IL-1β or Ccl5 inhibitors abrogates injury-induced glioma progression, thus establishing a causative relationship between injury and tumorigenesis.
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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.