ArticleOncotarget2016
Minimal contribution of ERK1/2-MAPK signalling towards the maintenance of oncogenic GNAQQ209P-driven uveal melanomas in zebrafish.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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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
22 citing papers in PubMed, 31 citations in OpenAlex.
- Electroporation with Calcium or Bleomycin: First Application in an In Vivo Uveal Melanoma Patient-Derived Xenograft Model.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Investigating the Role of DUSP4 in Uveal Melanoma.Translational vision science & technology · 2022Article
- Review
- MITF deficiency accelerates GNAQ-driven uveal melanoma.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Animal Models of Uveal Melanoma.Annals of eye science · 2022Article
- The Impact of Ultraviolet Radiation on the Aetiology and Development of Uveal Melanoma.Cancers · 2021Review
- Hindsight: Review of Preclinical Disease Models for the Development of New Treatments for Uveal Melanoma.Journal of Cancer · 2021Review
- Genetic Engineering of Zebrafish in Cancer Research.Cancers · 2020Review
- Review
- Mouse models of uveal melanoma: Strengths, weaknesses, and future directions.Pigment cell & melanoma research · 2020Review
- Uveal melanoma: progress in molecular biology and therapeutics.Therapeutic advances in medical oncology · 2020Review
- Molecular Characteristics of Uveal Melanoma: Insights from the Cancer Genome Atlas (TCGA) Project.Cancers · 2019Review
- Heterogeneity in Mitogen-Activated Protein Kinase (MAPK) Pathway Activation in Uveal Melanoma With Somatic GNAQ and GNA11 Mutations.Investigative ophthalmology & visual science · 2019Article
- The Melding of Drug Screening Platforms for Melanoma.Frontiers in oncology · 2019Review
- Uveal melanoma driver mutations in GNAQ/11 yield numerous changes in melanocyte biology.Pigment cell & melanoma research · 2018Article
- GNAQ and GNA11 mutations and downstream YAP activation in choroidal nevi.British journal of cancer · 2017Article
- Zebrafish as a Model Organism for the Development of Drugs for Skin Cancer.International journal of molecular sciences · 2017Review
- From fish bowl to bedside: The power of zebrafish to unravel melanoma pathogenesis and discover new therapeutics.Pigment cell & melanoma research · 2017Review
- Dysregulated GPCR Signaling and Therapeutic Options in Uveal Melanoma.Molecular cancer research : MCR · 2017Review
- The biology of uveal melanoma.Cancer metastasis reviews · 2017Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Mutations affecting Gαq proteins are pervasive in uveal melanoma (UM), suggesting they 'drive' UM pathogenesis. The ERK1/2-MAPK pathway is critical for cutaneous melanoma development and consequently an important therapeutic target. Defining the contribution of ERK1/2-MAPK signalling to UM development has been hampered by the lack of an informative animal model that spontaneously develops UM. Towards this end, we engineered transgenic zebrafish to express oncogenic GNAQQ209P in the melanocyte lineage. This resulted in hyperplasia of uveal melanocytes, but with no evidence of malignant progression, nor perturbation of skin melanocytes. Combining expression of oncogenic GNAQQ209P with p53 inactivation resulted in earlier onset and even more extensive hyperplasia of uveal melanocytes that progressed to UM. Immunohistochemistry revealed only weak immunoreactivity to phosphorylated (p)ERK1/2 in established uveal tumours-in contrast to strong immunoreactivity in oncogenic RAS-driven skin lesions-but ubiquitous positive staining for nuclear Yes-associated protein (YAP). Moreover, no changes were observed in pERK1/2 levels upon transient knockdown of GNAQ or phospholipase C-beta (PLC-β) inhibition in the majority of human UM cell lines we tested harbouring GNAQ mutations. In summary, our findings demonstrate a weak correlation between oncogenic GNAQQ209P mutation and sustained ERK1/2-MAPK activation, implying that ERK1/2 signalling is unlikely to be instrumental in the maintenance of GNAQQ209P-driven UMs.
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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.