ArticleNature communications2018
TRPV4 and KRAS and FGFR1 gain-of-function mutations drive giant cell lesions of the jaw.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
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
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 80 citations in OpenAlex.
- Update from the 5th Edition of the World Health Organization Classification of Head and Neck Tumors: Odontogenic and Maxillofacial Bone Tumours.Head and neck pathology · 2022Pooled it
- Deep learning for classification of aggressive versus non-aggressive central giant cell granuloma using whole-slide histopathology images.Virchows Archiv : an international journal of pathology · 2026Article
- 25+ Years of TRPV4: From Discovery to Translational Horizons.Research square · 2026Article
- Article
- Concurrence of FGFR1 mutations modulates oncogenesis in glioneuronal tumors.The EMBO journal · 2025Article
- Giant Cell Lesions of the Jaws: A Work on Current Concepts and Making Through a Working Classification.Head and neck pathology · 2024Observational
- DNA methylation profile discriminates sporadic giant cell granulomas of the jaws and cherubism from their giant cell-rich histological mimics.The journal of pathology. Clinical research · 2023Article
- Management of a rare mandibular giant cell tumor of bone by neoadjuvant denosumab therapy and surgery: A 4-year follow-up case report.International journal of surgery case reports · 2023Article
- Developing Models to PredictBiomedicines · 2023Article
- Brown Tumour in Chronic Kidney Disease: Revisiting an Old Disease with a New Perspective.Cancers · 2023Review
- [The new WHO classification of jaw tumours].Pathologie (Heidelberg, Germany) · 2023Review
- Oestrogen receptor expression distinguishes non-ossifying fibroma from other giant cell containing bone tumours.Virchows Archiv : an international journal of pathology · 2022Article
- Clinical and Radiologic Response of Central Giant Cell Granuloma to Denosumab: A 6-Year Prospective Observational Study.Calcified tissue international · 2022Observational
- De novoJournal of medical genetics · 2022Article
- Giant Cell Lesions of the Jaws Involving RASopathy Syndromes.Acta stomatologica Croatica · 2022Review
- TRPV4 induces apoptosis via p38 MAPK in human lung cancer cells.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2021Article
- H3.3 G34W Promotes Growth and Impedes Differentiation of Osteoblast-Like Mesenchymal Progenitors in Giant Cell Tumor of Bone.Cancer discovery · 2020Article
- [Giant cell tumor of bone : Morphology, molecular pathogenesis, and differential diagnosis].Der Pathologe · 2020Review
- [Molecular pathology in the diagnosis of bone tumors: current concepts].Der Pathologe · 2020Review
- Soft Tissue Special Issue: Giant Cell-Rich Lesions of the Head and Neck Region.Head and neck pathology · 2020Review
Corrections and comments
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Authors and funding
23 authors at 8 institutions in 5 countries.
Funding
Abstract
Giant cell lesions of the jaw (GCLJ) are debilitating tumors of unknown origin with limited available therapies. Here, we analyze 58 sporadic samples using next generation or targeted sequencing and report somatic, heterozygous, gain-of-function mutations in KRAS, FGFR1, and p.M713V/I-TRPV4 in 72% (42/58) of GCLJ. TRPV4 p.M713V/I mutations are exclusive to central GCLJ and occur at a critical position adjacent to the cation permeable pore of the channel. Expression of TRPV4 mutants in HEK293 cells leads to increased cell death, as well as increased constitutive and stimulated channel activity, both of which can be prevented using TRPV4 antagonists. Furthermore, these mutations induce sustained activation of ERK1/2, indicating that their effects converge with that of KRAS and FGFR1 mutations on the activation of the MAPK pathway in GCLJ. Our data extend the spectrum of TRPV4 channelopathies and provide rationale for the use of TRPV4 and RAS/MAPK antagonists at the bedside in GCLJ.
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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.