ArticleCell death & disease2025
Identification of targetable epigenetic vulnerabilities for uveal melanoma.
Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Establishment of Uveal Melanoma Patient-Derived Organoids Using an Air-Liquid Interface System for Translational Research.Investigative ophthalmology & visual science · 2026Article
- Current Research in Polypharmacology for Cancer Treatment Using Dual-Target Histone Deacetylase Inhibitors.International journal of molecular sciences · 2026Review
- Uveal Melanoma: Biology, Prognostication, and Emerging Therapies to Outsmart an Immune-Cold Melanoma.Cancers · 2026Review
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Authors and funding
19 authors.
Funding
Abstract
Uveal melanoma (UM) is the most common adult primary intraocular malignancy, with a strong predilection for hepatic metastasis, occurring in approximately 50% of cases. Metastatic UM is highly resistant to therapy and is almost invariably fatal. The strongest genetic driver of UM metastasis is loss of function of the tumor suppressor BRCA-associated protein 1 (BAP1), which leads to widespread epigenetic dysregulation. To identify novel therapeutic strategies, we investigated whether targeting the epigenome of UM could reveal new vulnerabilities. We performed a high-throughput compound screen using a curated epigenetic inhibitor library and identified BET (bromodomain and extra-terminal domain) inhibition as a particularly promising approach. While previous clinical trials with BET inhibitors for UM treatment have failed, we found substantial heterogeneity in the efficacy of different BET inhibitors in UM. Notably, the BET inhibitor mivebresib (ABBV-075) significantly improved survival rates by 50% in a metastatic UM xenograft mouse model and prevented detectable metastases in the bones, spinal cord, and brain. Transcriptomic analysis revealed a strong overlap between BET and histone deacetylase (HDAC) inhibition, an approach currently under clinical evaluation for UM treatment. BET and HDAC inhibitors reversed gene expression signatures associated with high metastatic risk and induced a neuron-like phenotype in UM cells. These findings establish BET inhibition as a potent and previously underappreciated vulnerability for metastatic UM.
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Registered trials
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