ArticleNature communications2023
MEK inhibition reduced vascular tumor growth and coagulopathy in a mouse model with hyperactive GNAQ.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 26 citations in OpenAlex.
- Review
- Analysis of Phosphorylated MEK1 Expression Pattern in Cutaneous Dilated Vessels of Capillary Malformations.The Journal of dermatology · 2026Article
- Acute Seizure Susceptibility and Chronic Vascular Malformation in a Developmental Mouse Model of Sturge-Weber Syndrome.International journal of molecular sciences · 2026Article
- MEK Inhibition Reduces Vascular Malformations and Gene Dysregulation in NRASPediatric blood & cancer · 2026Article
- Calcineurin-NFAT-DSCR1.4 signaling as druggable axis in Gαq-R183Q-driven capillary malformations.Angiogenesis · 2026Article
- Vascular Organoids Derived from Capillary malformation-induced Pluripotent Stem Cells Exhibit Disease-Relevant Phenotypes.Stem cell reviews and reports · 2026Article
- MAPK signaling and angiopoietin-2 contribute to endothelial permeability in capillary malformations.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- An endothelial specific mouse model for the capillary malformation mutation Gnaq p.R183Q.Angiogenesis · 2025Article
- Transcriptomic Profiling Unveils EDN3Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- R183Q GNAQ Sturge-Weber syndrome Leptomeningeal and Cerebrovascular Developmental Mouse Model.Journal of vascular anomalies · 2024Article
- GNA14 and GNAQ somatic mutations cause spinal and intracranial extra-axial cavernous hemangiomas.American journal of human genetics · 2024Article
- NRASPediatric blood & cancer · 2024Article
- Capillary malformations.The Journal of clinical investigation · 2024Review
- Chitosan-based thermosensitive hydrogel with long-term release of murine nerve growth factor for neurotrophic keratopathy.Neural regeneration research · 2024Article
- Sturge-Weber syndrome: updates in translational neurology.Frontiers in neurology · 2024Review
- Oncogenic Gαq activates RhoJ through PDZ-RhoGEF.International journal of molecular sciences · 2023Article
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Authors and funding
13 authors at 2 institutions in 2 countries.
Funding
Abstract
Activating non-inherited mutations in the guanine nucleotide-binding protein G(q) subunit alpha (GNAQ) gene family have been identified in childhood vascular tumors. Patients experience extensive disfigurement, chronic pain and severe complications including a potentially lethal coagulopathy termed Kasabach-Merritt phenomenon. Animal models for this class of vascular tumors do not exist. This has severely hindered the discovery of the molecular consequences of GNAQ mutations in the vasculature and, in turn, the preclinical development of effective targeted therapies. Here we report a mouse model expressing hyperactive mutant GNAQ in endothelial cells. Mutant mice develop vascular and coagulopathy phenotypes similar to those seen in patients. Mechanistically, by transcriptomic analysis we demonstrate increased mitogen activated protein kinase signaling in the mutant endothelial cells. Targeting of this pathway with Trametinib suppresses the tumor growth by reducing vascular cell proliferation and permeability. Trametinib also prevents the development of coagulopathy and improves mouse survival.
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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 Socratic graph.