ArticleGenes & development1999
Schwann cell hyperplasia and tumors in transgenic mice expressing a naturally occurring mutant NF2 protein.
Article in Genes & development, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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.
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Who cites it
55 citing papers in PubMed, 144 citations in OpenAlex.
- Stereotactic radiosurgery for NF2-related schwannomatosis and schwannomatosis-associated spinal tumors: a single-institution cohort.Journal of spine surgery (Hong Kong) · 2026Article
- Quantitative imaging of schwannoma captures heterogeneity and accelerates preclinical testing, revealing distinct impacts of targeted therapies.bioRxiv : the preprint server for biology · 2026Article
- Focused ultrasound-mediated drug delivery of bevacizumab in treating NF2-related schwannomatosis in an animal model.Scientific reports · 2025Article
- Pathologic and Therapeutic Schwann Cells.Cells · 2025Review
- Genetics and current research models of Mendelian tumor predisposition syndromes with ocular involvement.Progress in retinal and eye research · 2025Review
- Current molecular understanding of central nervous system schwannomas.Acta neuropathologica communications · 2025Review
- Targeted STAT1 therapy for LZTR1-driven peripheral nerve sheath tumor.Cancer communications (London, England) · 2023Article
- Missense variant interaction scanning reveals a critical role of the FERM domain for tumor suppressor protein NF2 conformation and function.Life science alliance · 2023Article
- The genetic landscape and possible therapeutics of neurofibromatosis type 2.Cancer cell international · 2023Review
- Cellular mechanisms of heterogeneity in NF2-mutant schwannoma.Nature communications · 2023Article
- Heterogeneity and Potency of Peripheral Glial Cells in Embryonic Development and Adults.Frontiers in molecular neuroscience · 2022Review
- Current Understanding of Neurofibromatosis Type 1, 2, and Schwannomatosis.International journal of molecular sciences · 2021Review
- Genetic Events and Signaling Mechanisms Underlying Schwann Cell Fate in Development and Cancer.Neurosurgery · 2021Review
- Combination therapy with mTOR kinase inhibitor and dasatinib as a novel therapeutic strategy for vestibular schwannoma.Scientific reports · 2020Article
- Neurogenesis From Neural Crest Cells: Molecular Mechanisms in the Formation of Cranial Nerves and Ganglia.Frontiers in cell and developmental biology · 2020Review
- Phosphorylation of Merlin by Aurora A kinase appears necessary for mitotic progression.The Journal of biological chemistry · 2019Article
- Preclinical assessment of MEK1/2 inhibitors for neurofibromatosis type 2-associated schwannomas reveals differences in efficacy and drug resistance development.Neuro-oncology · 2019Article
- A cerebellopontine angle mouse model for the investigation of tumor biology, hearing, and neurological function in NF2-related vestibular schwannoma.Nature protocols · 2019Article
- Nf2 Mutation in Schwann Cells Delays Functional Neural Recovery Following Injury.Neuroscience · 2018Article
- Timing of Smarcb1 and Nf2 inactivation determines schwannoma versus rhabdoid tumor development.Nature communications · 2017Article
Corrections and comments
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Authors and funding
9 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Specific mutations in some tumor suppressor genes such as p53 can act in a dominant fashion. We tested whether this mechanism may also apply for the neurofibromatosis type-2 gene (NF2) which, when mutated, leads to schwannoma development. Transgenic mice were generated that express, in Schwann cells, mutant NF2 proteins prototypic of natural mutants observed in humans. Mice expressing a NF2 protein with an interstitial deletion in the amino-terminal domain showed high prevalence of Schwann cell-derived tumors and Schwann cell hyperplasia, whereas those expressing a carboxy-terminally truncated protein were normal. Our results indicate that a subset of mutant NF2 alleles observed in patients may encode products with dominant properties when overexpressed in specific cell lineages.
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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.