ArticleCancers2022
Introduction of Mutant GNAQ into Endothelial Cells Induces a Vascular Malformation Phenotype with Therapeutic Response to Imatinib.
Article in Cancers, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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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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
8 citing papers in PubMed, 13 citations in OpenAlex.
- R183Q GNAQ Sturge-Weber syndrome Leptomeningeal and Cerebrovascular Developmental Mouse Model.Journal of vascular anomalies · 2024Article
- Sturge-Weber syndrome: an update for the pediatrician.World journal of pediatrics : WJP · 2024Review
- Capillary malformations.The Journal of clinical investigation · 2024Review
- Nilotinib-induced alterations in endothelial cell function recapitulate clinical vascular phenotypes independent of ABL1.Scientific reports · 2024Article
- Article
- Targeting the Vulnerabilities of Oncogene Activation.Cancers · 2023Article
- Perivascular localized cells commit erythropoiesis in PDGF-B-expressing solid tumors.Cancer communications (London, England) · 2023Article
- Indolium 1 Exerts Activity against Vemurafenib-Resistant Melanoma In Vivo.Antioxidants (Basel, Switzerland) · 2022Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
GNAQ is mutated in vascular and melanocytic lesions, including vascular malformations and nevi. No in vivo model of GNAQ activation in endothelial cells has previously been described. We introduce mutant GNAQ into a murine endothelial cell line, MS1. The resultant transduced cells exhibit a novel phenotype in vivo, with extensive vasoformative endothelial cells forming aberrant lumens similar to those seen in vascular malformations. ATAC-seq analysis reveals activation of c-Kit in the novel vascular malformations. We demonstrate that c-Kit is expressed in authentic human Sturge-Weber vascular malformations, indicating a novel druggable target for Sturge-Weber syndrome. Since c-Kit is targeted by the FDA-approved drug imatinib, we tested the ability of imatinib on the phenotype of the vascular malformations in vivo. Imatinib treated vascular malformations are significantly smaller and have decreased supporting stromal cells surrounding the lumen. Imatinib may be useful in the treatment of human vascular malformations that express c-Kit, including Sturge-Weber syndrome.
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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.