New Insights into the Exosome-Induced Migration of Uveal Melanoma Cells and the Pre-Metastatic Niche Formation in the Liver.

UM is an aggressive intraocular tumor characterized by high plasticity and a propensity to metastasize in the liver. However, the underlying mechanisms governing liver tropism remain poorly understood. Given the emerging significance of exosomes, we sought to investigate the contribution of UM-derived exosomes to specific steps of the metastatic process.

[Translated article] Changes in the Location of Cutaneous Melanoma Over the Past 30 Years. A Retrospective Observational Study.

Background: The location of cutaneous melanoma is associated with photoexposure.

Objectives: To retrospectively analyze changes in the location of cutaneous melanoma over the past 30 years.

Patients And Methods: All patients treated at our hospital for cutaneous melanoma from 1988 through 2017 were prospectively collected.

PRRX1 silencing is required for metastatic outgrowth in melanoma and is an independent prognostic of reduced survival in patients.

Paired related homeobox 1 (PRRX1) is an inducer of epithelial-to-mesenchymal transition (EMT) in different types of cancer cells. We detected low PRRX1 expression in nevus but increased levels in primary human melanoma and cell lines carrying the BRAF mutation. High expression of PRRX1 correlates with invasiveness and enrichment of genes belonging to the EMT programme.

Orthotopic murine xenograft model of uveal melanoma with spontaneous liver metastasis.

Uveal melanoma is the most common intraocular malignancy in adults. Despite the effective primary treatment, up to 50% of patients with uveal melanoma will develop metastatic lesions mainly in the liver, which are resistant to conventional chemotherapy and lead to patient's death. To date, no orthotopic murine models of uveal melanoma which can develop spontaneous metastasis are available for preclinical studies.

Oncogenic properties via MAPK signaling of the SOX5-RAF1 fusion gene identified in a wild-type NRAS/BRAF giant congenital nevus.

We recently reported an RAF rearrangement without NRAS or BRAF mutations in lesions from Giant Congenital Melanocytic Nevi (CMN). The new gene fusion involves the 5'-end of the promoter-containing N terminus of the SOX5 gene fused to exons 7-16 of the 3'-end of RAF1 gene leading to a SOX5-RAF1 fusion transcript which loses the auto-inhibitory CR1 domain but retains the complete in-frame coding sequence for the C-Terminal kinase domain of the RAF1. Stable expression of SOX5-RAF1 fusion induced growth factor-independent cell growth in murine hematopoietic Ba/F3 cells and melan-a immortalized melanocytes.