{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Zhang Y"],"funding":["National Institutes of Health National Cancer Institute","University of Utah","University of California, San Francisco","NCI NIH HHS","US Department of Defense","National Institutes of Health","NIH HHS","Elsa U Pardee Foundation"],"pagination":["116675"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12834598"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["44(12)"],"pubmed_abstract":["Metastatic spread and therapeutic resistance are the principal causes of cancer mortality. For melanoma, these processes rely on the capacity of cells to switch between transcriptional states. Although targeting transcriptional states pharmacologically is promising, the mechanisms by which melanoma cells switch between states-and how these processes differ from melanocytes-remain poorly understood. Here, we isolate distinct melanoma states with unique phenotypes: a MYC-driven state, essential for tumor initiation yet sensitive to BRAF inhibition, and a dedifferentiated, invasive BRN2-high state enriched in therapy-resistant cells but not directly tumorigenic. Transitions between phenotypes occur through intermediate, more differentiated states. Unexpectedly, the BRN2-high state is also pre"],"journal":["Cell reports"],"pubmed_title":["A BRN2:MYC transcriptional axis regulates interconversion between therapy-resistant and tumorigenic phenotypes in melanoma."],"pmcid":["PMC12834598"],"funding_grant_id":["R01 CA229896","R01CA276653","W81XWH2010530","R01 CA276653","W81XWH2210495","R01CA229896","CA-0122861","DP5 OD019787","P30CA042014"],"pubmed_authors":["Deacon DC","Lieberman M","Neuendorf HM","Zangle TA","Urquijo MA","Grossman D","Liu T","Mehrabad EM","Becker CA","Done A","Ferita M","Weinberger LS","Chang M","Kulkarni R","Lange D","Reeves MQ","Hansen MMK","Hejna M","Marks K","Stubben CJ","Smith EA","Lohman BK","Judson-Torres RL","Zitnay RG","Belote RL","Zhang Y","Spike BT","Zhang X","Hu M","Vand-Rajabpour F","VanBrocklin MW","Boyle GM","Moustafa TE","Lex A"],"additional_accession":[]},"is_claimable":false,"name":"A BRN2:MYC transcriptional axis regulates interconversion between therapy-resistant and tumorigenic phenotypes in melanoma.","description":"Metastatic spread and therapeutic resistance are the principal causes of cancer mortality. For melanoma, these processes rely on the capacity of cells to switch between transcriptional states. Although targeting transcriptional states pharmacologically is promising, the mechanisms by which melanoma cells switch between states-and how these processes differ from melanocytes-remain poorly understood. Here, we isolate distinct melanoma states with unique phenotypes: a MYC-driven state, essential for tumor initiation yet sensitive to BRAF inhibition, and a dedifferentiated, invasive BRN2-high state enriched in therapy-resistant cells but not directly tumorigenic. Transitions between phenotypes occur through intermediate, more differentiated states. Unexpectedly, the BRN2-high state is also pre","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Dec","modification":"2026-07-15T09:07:32.207Z","creation":"2026-07-02T03:08:51.842Z"},"accession":"S-EPMC12834598","cross_references":{"pubmed":["41405996"],"doi":["10.1016/j.celrep.2025.116675"]}}