{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"submitter":["Smith EA"],"funding":["NCI NIH HHS"],"pubmed_abstract":["Acral melanoma (AM) is an aggressive melanoma variant that arises from palmar, plantar, and nail unit melanocytes. Compared to non-acral cutaneous melanoma (CM), AM is biologically distinct, has an equal incidence across genetic ancestries, typically presents in advanced stage disease, is less responsive to therapy, and has an overall worse prognosis. Independent analysis of published genomic and transcriptomic sequencing identified that receptor tyrosine kinase (RTK) ligands and adapter proteins are frequently amplified, translocated, and/or overexpressed in AM. To target these unique genetic changes, a zebrafish acral melanoma model was exposed to a panel of narrow and broad spectrum multi-RTK inhibitors, revealing that dual FGFR/VEGFR inhibitors decrease acral-analogous melanocyte proli"],"journal":["bioRxiv : the preprint server for biology"],"pagination":["2024.06.15.599116"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11212935"],"repository":["biostudies-literature"],"pubmed_title":["Receptor tyrosine kinase inhibition leads to regression of acral melanoma by targeting the tumor microenvironment."],"pmcid":["PMC11212935"],"funding_grant_id":["P30 CA042014","R01 CA276653"],"pubmed_authors":["Deacon DC","Balatico M","Zangle TA","Grossmann AH","Smith EA","Chan TY","Lum DH","Judson-Torres RL","Belote RL","Hyngstrom JR","Seasor TA","Alizada S","Becker CA","Jiang A","Cortes-Sanchez E","Cruz NM","Zeng H","Moustafa TE","White RM"],"additional_accession":[]},"is_claimable":false,"name":"Receptor tyrosine kinase inhibition leads to regression of acral melanoma by targeting the tumor microenvironment.","description":"Acral melanoma (AM) is an aggressive melanoma variant that arises from palmar, plantar, and nail unit melanocytes. Compared to non-acral cutaneous melanoma (CM), AM is biologically distinct, has an equal incidence across genetic ancestries, typically presents in advanced stage disease, is less responsive to therapy, and has an overall worse prognosis. Independent analysis of published genomic and transcriptomic sequencing identified that receptor tyrosine kinase (RTK) ligands and adapter proteins are frequently amplified, translocated, and/or overexpressed in AM. To target these unique genetic changes, a zebrafish acral melanoma model was exposed to a panel of narrow and broad spectrum multi-RTK inhibitors, revealing that dual FGFR/VEGFR inhibitors decrease acral-analogous melanocyte proli","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Jun","modification":"2025-04-22T15:29:26.451Z","creation":"2025-04-06T01:24:30.963Z"},"accession":"S-EPMC11212935","cross_references":{"pubmed":["38948879"],"doi":["10.1101/2024.06.15.599116"]}}