{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["15"],"submitter":["Muraro E"],"pubmed_abstract":["<h4>Introduction</h4>About 50% of cutaneous melanoma (CM) patients present activating BRAF mutations that can be effectively targeted by BRAF inhibitors (BRAFi). However, 20% of CM patients exhibit intrinsic drug resistance to BRAFi, while most of the others develop adaptive resistance over time. The mechanisms involved in BRAFi resistance are disparate and globally seem to rewire the cellular signaling profile by up-regulating different receptor tyrosine kinases (RTKs), such as the epidermal growth factor receptor (EGFR). RTKs inhibitors have not clearly demonstrated anti-tumor activity in BRAFi resistant models. To overcome this issue, we wondered whether the shared up-regulated RTK phenotype associated with BRAFi resistance could be exploited by using immune weapons as the antibody-depe"],"journal":["Frontiers in immunology"],"pagination":["1336566"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10950948"],"repository":["biostudies-literature"],"pubmed_title":["Antibody dependent cellular cytotoxicity-inducing anti-EGFR antibodies as effective therapeutic option for cutaneous melanoma resistant to BRAF inhibitors."],"pmcid":["PMC10950948"],"pubmed_authors":["Canzonieri V","Anichini A","Giurato G","Sigalotti L","Montico B","Mortarini R","Lum B","Rizzo A","Simpson F","Fratta E","Guerrieri R","Comaro E","Colizzi F","Dolcetti R","Muraro E","Del Vecchio M","Salvati A","Milione M","Weisz A","Pizzichetta MA"],"additional_accession":[]},"is_claimable":false,"name":"Antibody dependent cellular cytotoxicity-inducing anti-EGFR antibodies as effective therapeutic option for cutaneous melanoma resistant to BRAF inhibitors.","description":"<h4>Introduction</h4>About 50% of cutaneous melanoma (CM) patients present activating BRAF mutations that can be effectively targeted by BRAF inhibitors (BRAFi). However, 20% of CM patients exhibit intrinsic drug resistance to BRAFi, while most of the others develop adaptive resistance over time. The mechanisms involved in BRAFi resistance are disparate and globally seem to rewire the cellular signaling profile by up-regulating different receptor tyrosine kinases (RTKs), such as the epidermal growth factor receptor (EGFR). RTKs inhibitors have not clearly demonstrated anti-tumor activity in BRAFi resistant models. To overcome this issue, we wondered whether the shared up-regulated RTK phenotype associated with BRAFi resistance could be exploited by using immune weapons as the antibody-depe","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024","modification":"2026-07-15T09:26:46.424Z","creation":"2025-06-01T00:31:21.734Z"},"accession":"S-EPMC10950948","cross_references":{"pubmed":["38510242"],"doi":["10.3389/fimmu.2024.1336566"]}}