ArticleOncotarget2017
The cell of origin dictates the temporal course of neurofibromatosis-1 (Nf1) low-grade glioma formation.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 36 citations in OpenAlex.
- Nested ecosystems theory for conceptualizing brain tumors.Disease models & mechanisms · 2026Review
- Aberrant coupling of glutamate and tyrosine kinase receptors enables neuronal control of brain-tumor growth.Neuron · 2025Article
- Current states in understanding oligodendroglia-mediated neurological issues in neurofibromatosis type 1 (NF1).Acta neuropathologica communications · 2025Review
- Genetics and current research models of Mendelian tumor predisposition syndromes with ocular involvement.Progress in retinal and eye research · 2025Review
- Maternal obesogenic diet operates at the tumor cell of origin to increase incidence and decrease latency of neurofibromatosis type 1 optic pathway glioma.Neuro-oncology · 2024Article
- Single cell spatial biology over developmental time can decipher pediatric brain pathologies.Neurobiology of disease · 2024Review
- Nf1 mutation disrupts activity-dependent oligodendroglial plasticity and motor learning in mice.Nature neuroscience · 2024Article
- An Overview of Optic Pathway Glioma With Neurofibromatosis Type 1: Pathogenesis, Risk Factors, and Therapeutic Strategies.Investigative ophthalmology & visual science · 2024Review
- Visual Deficits and Diagnostic and Therapeutic Strategies for Neurofibromatosis Type 1: Bridging Science and Patient-Centered Care.Vision (Basel, Switzerland) · 2024Review
- Review
- Optimizing preclinical pediatric low-grade glioma models for meaningful clinical translation.Neuro-oncology · 2023Article
- The Neuroimmune Regulation and Potential Therapeutic Strategies of Optic Pathway Glioma.Brain sciences · 2023Review
- Retinal ganglion cell repopulation for vision restoration in optic neuropathy: a roadmap from the RReSTORe Consortium.Molecular neurodegeneration · 2023Review
- Pediatric low-grade glioma models: advances and ongoing challenges.Frontiers in oncology · 2023Review
- Neurofibromatosis Type 1-Associated Optic Pathway Gliomas: Current Challenges and Future Prospects.Cancer management and research · 2023Review
- Multiplatform molecular analyses refine classification of gliomas arising in patients with neurofibromatosis type 1.Acta neuropathologica · 2022Article
- Neuron-Glial Interactions in Health and Brain Cancer.Advanced biology · 2022Review
- Human induced pluripotent stem cell engineering establishes a humanized mouse platform for pediatric low-grade glioma modeling.Acta neuropathologica communications · 2022Article
- Reimagining pilocytic astrocytomas in the context of pediatric low-grade gliomas.Neuro-oncology · 2021Review
- Temporal, spatial, and genetic constraints contribute to the patterning and penetrance of murine neurofibromatosis-1 optic glioma.Neuro-oncology · 2021Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Low-grade gliomas are one of the most common brain tumors in children, where they frequently form within the optic pathway (optic pathway gliomas; OPGs). Since many OPGs occur in the context of the Neurofibromatosis Type 1 (NF1) cancer predisposition syndrome, we have previously employed Nf1 genetically-engineered mouse (GEM) strains to study the pathogenesis of these low-grade glial neoplasms. In the light of the finding that human and mouse low-grade gliomas are composed of Olig2+ cells and that Olig2+ oligodendrocyte precursor cells (OPCs) give rise to murine high-grade gliomas, we sought to determine whether Olig2+ OPCs could be tumor-initiating cells for Nf1 optic glioma. Similar to the GFAP-Cre transgenic strain previously employed to generate Nf1 optic gliomas, Olig2+ cells also give rise to astrocytes in the murine optic nerve in vivo. However, in contrast to the GFAP-Cre strain where somatic Nf1 inactivation in embryonic neural progenitor/stem cells (Nf1flox/mut; GFAP-Cre mice) results in optic gliomas by 3 months of age in vivo, mice with Nf1 gene inactivation in Olig2+ OPCs (Nf1flox/mut; Olig2-Cre mice) do not form optic gliomas until 6 months of age. These distinct patterns of glioma latency do not reflect differences in the timing or brain location of somatic Nf1 loss. Instead, they most likely reflect the cell of origin, as somatic Nf1 loss in CD133+ neural progenitor/stem cells during late embryogenesis results in optic gliomas at 3 months of age. Collectively, these data demonstrate that the cell of origin dictates the time to tumorigenesis in murine optic glioma.
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