ArticleOncogene2014
NG2-cells are not the cell of origin for murine neurofibromatosis-1 (Nf1) optic glioma.
Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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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.
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Who cites it
22 citing papers in PubMed, 28 citations in OpenAlex.
- An Overview of Optic Pathway Glioma With Neurofibromatosis Type 1: Pathogenesis, Risk Factors, and Therapeutic Strategies.Investigative ophthalmology & visual science · 2024Review
- Single-cell transcriptomic analysis identifies downregulated phosphodiesterase 8B as a novel oncogene in IDH-mutant glioma.Frontiers in immunology · 2024Article
- 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
- Pediatric low-grade glioma models: advances and ongoing challenges.Frontiers in oncology · 2023Review
- Neuron-Glial Interactions in Health and Brain Cancer.Advanced biology · 2022Review
- 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
- The cell of origin dictates the temporal course of neurofibromatosis-1 (Nf1) low-grade glioma formation.Oncotarget · 2017Article
- Simultaneous detection of mRNA transcription and decay intermediates by dual colour single mRNA FISH on subcellular resolution.Nucleic acids research · 2017Article
- NF1 germline mutation differentially dictates optic glioma formation and growth in neurofibromatosis-1.Human molecular genetics · 2016Article
- RNA Sequencing of Tumor-Associated Microglia Reveals Ccl5 as a Stromal Chemokine Critical for Neurofibromatosis-1 Glioma Growth.Neoplasia (New York, N.Y.) · 2015Article
- RASopathies: unraveling mechanisms with animal models.Disease models & mechanisms · 2015Review
- Akt- or MEK-mediated mTOR inhibition suppresses Nf1 optic glioma growth.Neuro-oncology · 2015Article
- Transformation of quiescent adult oligodendrocyte precursor cells into malignant glioma through a multistep reactivation process.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Eliminating barriers to personalized medicine: learning from neurofibromatosis type 1.Neurology · 2014Review
- Review
- CTF meeting 2012: Translation of the basic understanding of the biology and genetics of NF1, NF2, and schwannomatosis toward the development of effective therapies.American journal of medical genetics. Part A · 2014Article
- Conditional KIAA1549:BRAF mice reveal brain region- and cell type-specific effects.Genesis (New York, N.Y. : 2000) · 2013Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Low-grade glial neoplasms (astrocytomas) represent one of the most common brain tumors in the pediatric population. These tumors frequently form in the optic pathway (optic pathway gliomas, OPGs), especially in children with the neurofibromatosis type 1 (NF1)-inherited tumor predisposition syndrome. To model these tumors in mice, we have previously developed several Nf1 genetically-engineered mouse strains that form optic gliomas. However, there are three distinct macroglial cell populations in the optic nerve (astrocytes, NG2+ (nerve/glial antigen 2) cells and oligodendrocytes). The presence of NG2+ cells in the optic nerve raises the intriguing possibility that these cells could be the tumor-initiating cells, as has been suggested for adult glioma. In this report, we used a combination of complementary in vitro and novel genetically-engineered mouse strains in vivo to determine whether NG2+ cells could give rise to Nf1 optic glioma. First, we show that Nf1 inactivation results in a cell-autonomous increase in glial fibrillary acidic protein+ (GFAP+), but not in NG2+, cell proliferation in vitro. Second, similar to the GFAP-Cre transgenic strain that drives Nf1 optic gliomagenesis, NG2-expressing cells also give rise to all three macroglial lineages in vivo. Third, in contrast to the GFAP-Cre strain, Nf1 gene inactivation in NG2+ cells is not sufficient for optic gliomagenesis in vivo. Collectively, these data demonstrate that NG2+ cells are not the cell of origin for mouse optic glioma, and support a model in which gliomagenesis requires Nf1 loss in specific neuroglial progenitors during embryogenesis.
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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.