ArticleNature communications2017
Timing of Smarcb1 and Nf2 inactivation determines schwannoma versus rhabdoid tumor development.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
60 citing papers in PubMed, 1 synthesis or guideline pooled it, 100 citations in OpenAlex.
- Molecular subgrouping of atypical teratoid/rhabdoid tumors-a reinvestigation and current consensus.Neuro-oncology · 2020Pooled it
- Variable latency between the founder genetic event and rhabdoid tumor expansion.bioRxiv : the preprint server for biology · 2026Article
- Development of a Genetically Engineered Porcine Model of Rhabdoid Tumor Predisposition Syndrome Type 1 (RTPS-1).Cancers · 2026Article
- Deciphering and Targeting the Schwannoma-Neuron-Macrophage Crosstalk for the Treatment of Schwannomatosis and Associated Pain.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Quantitative imaging of schwannoma captures heterogeneity and accelerates preclinical testing, revealing distinct impacts of targeted therapies.bioRxiv : the preprint server for biology · 2026Article
- Schwannomatosis tumor modeling: progress and prospects for translational research.Journal of biological engineering · 2026Review
- Histogenesis of Atypical Teratoid Rhabdoid Tumors: Anatomical and Embryological Perspectives.Cancers · 2025Article
- A cycling, progenitor-like cell population at the base of atypical teratoid rhabdoid tumor subtype differentiation trajectories.Neuro-oncology · 2025Article
- Identification of therapeutic targets for renal medullary carcinoma via integrated genomic and transcriptomic profiling.Cell reports. Medicine · 2025Article
- SMARCB1-related schwannomatosis and other SMARCB1-associated phenotypes: clinical spectrum and molecular pathogenesis.Familial cancer · 2025Review
- Gene therapy and genome-editing for schwannoma in NF2-related schwannomatosis: current understanding and future directions.Journal of neuro-oncology · 2025Review
- SMARCB1-deficient malignant melanocytic uveal tumours: a new neural crest-derived tumour entity with SMARCB1-related germline predisposition.The Journal of pathology · 2025Article
- Analysis of ABCC3 in glioma progression: implications for prognosis, immunotherapy, and drug resistance.Discover oncology · 2025Article
- A four-hit mechanism is sufficient for meningioma development.Journal of neuro-oncology · 2025Article
- WWC proteins-mediated compensatory mechanism restricts schwannomatosis driven byScience advances · 2025Article
- Mapping the Somatic Mutation Landscape of Familial NF2-Related Schwannomatosis using Whole-Exome Sequencing.International journal of medical sciences · 2025Article
- Optimal Delivery of Pain Management in Schwannomatosis: A Literature Review.Therapeutics and clinical risk management · 2025Review
- Role ofCancers · 2024Review
- Functional screening reveals genetic dependencies and diverging cell cycle control in atypical teratoid rhabdoid tumors.Genome biology · 2024Article
- Typical NF2 and LTZR1 mutations are retained in an immortalized human schwann cell model of schwannomatosis.Heliyon · 2024Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Germline mutations of the SMARCB1 gene predispose to two distinct tumor syndromes: rhabdoid tumor predisposition syndrome, with malignant pediatric tumors mostly developing in brain and kidney, and familial schwannomatosis, with adulthood benign tumors involving cranial and peripheral nerves. The mechanisms by which SMARCB1 germline mutations predispose to rhabdoid tumors versus schwannomas are still unknown. Here, to understand the origin of these two types of SMARCB1-associated tumors, we generated different tissue- and developmental stage-specific conditional knockout mice carrying Smarcb1 and/or Nf2 deletion. Smarcb1 loss in early neural crest was necessary to initiate tumorigenesis in the cranial nerves and meninges with typical histological features and molecular profiles of human rhabdoid tumors. By inducing Smarcb1 loss at later developmental stage in the Schwann cell lineage, in addition to biallelic Nf2 gene inactivation, we generated the first mouse model developing schwannomas with the same underlying gene mutations found in schwannomatosis patients. SMARCB1 mutations predispose to rhabdoid tumors and schwannomas but the mechanisms underlying the tumor type specificity are unknown. Here the authors present new mouse models and show that early Smarcb1 loss causes rhabdoid tumors whereas loss at later stages combined with Nf2 gene inactivation causes shwannomas.
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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.