ArticleScientific reports2019
Multi-Platform Omics Analysis for Identification of Molecular Characteristics and Therapeutic Targets of Uveal Melanoma.
Article in Scientific reports, 2019. 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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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- A Multistep Immune-Competent Genetically Engineered Mouse Model Reveals Phenotypic Plasticity in Uveal Melanoma.Cancer research · 2026Article
- A multi-step immune-competent genetic mouse model reveals phenotypic plasticity in uveal melanoma.bioRxiv : the preprint server for biology · 2025Article
- PRAME Expression: A Target for Cancer Immunotherapy and a Prognostic Factor in Uveal Melanoma.Investigative ophthalmology & visual science · 2023Article
- MITF deficiency accelerates GNAQ-driven uveal melanoma.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Novel Therapeutic Approaches with DNA Damage Response Inhibitors for Melanoma Treatment.Cells · 2022Review
- Coexisting and Second Primary Cancers in Patients with Uveal Melanoma: A 10-Year Nationwide Database Analysis.Journal of clinical medicine · 2021Article
- Review
- Changes in microRNA expression associated with metastasis and survival in patients with uveal melanoma.Oncotarget · 2020Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Currently, there is no effective treatment for metastatic uveal melanoma (UVM). Here, we aimed to identify the mechanism involving intrinsic chemoresistance of metastatic UVM and the relevant therapeutic targets for UVM. We analyzed cohorts of 80 and 67 patients with primary UVM and skin cutaneous melanoma (SKCM), respectively, using The Cancer Genome Atlas dataset. Mutational burdens identified by whole exome sequencing were significantly lower in UVM than in SKCM patients. COSMIC mutational signature analysis identified that most of the mutations in UVM patients (>90%) were associated with spontaneous deamination of 5-methylcytosine or defective mismatch repair. Transcriptome analysis revealed that the MYC signature was more enriched in UVM patients, as compared to SKCM patients. Fifty-nine (73.8%) of 80 UVM patients showed gains in MYC copy number, and a high MYC copy number was associated with aggressive clinicopathological features of tumors and poor survival. Kinome-wide siRNA library screening identified several therapeutic targets, reported as synthetic lethal targets for MYC-addicted cancers. Notably, UVM cell lines showed high susceptibility to a WEE1 inhibitor (MK-1775; adavosertib) at a clinically tolerable dose. Overall, our study identified high MYC activity in UVM, and suggested G2/M checkpoint inhibitors as effective therapeutic targets for UVM.
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Registered trials
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