title: A STATement on vemurafenib-resistant melanoma.
abstract: Despite recent advancements in the treatment of late-stage mutant BRAF (V600E/K) melanomas, a major hurdle continues to be acquired resistance to BRAF inhibitors such as vemurafenib. The mechanisms for resistance have proven to be heterogeneous, emphasizing the need to use broad therapeutic approaches. In this issue, the study "Stat3-targeted therapies overcome the acquired resistance to vemurafenib in melanomas" by Liu et al. proposes that signal transducer and activator of transcription 3 (STAT3)-paired box 3 (PAX3) signaling may be a mechanism that is used by melanomas to resist RAF inhibitors.
authors.affiliation: Department of Cancer Biology and Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA. ejh004@Jefferson.edu
authors.forename: Edward J
authors.initials: EJ
authors.lastname: Hartsough
authors.forename: Andrew E
authors.initials: AE
authors.lastname: Aplin
mesh_terms: D019008:Drug Resistance, Neoplasm / Q000502:physiology*; D006801:Humans; D007211:Indoles / Q000494:pharmacology*; D015603:Keratinocytes / Q000187:drug effects*; D008297:Male; D008545:Melanoma / Q000188:drug therapy*; D050796:STAT3 Transcription Factor / Q000037:antagonists & inhibitors*; D012878:Skin Neoplasms / Q000188:drug therapy*; D013449:Sulfonamides / Q000494:pharmacology*; D000077484:Vemurafenib
chemical_list: D007211:Indoles; D050796:STAT3 Transcription Factor; C494086:STAT3 protein, human; D013449:Sulfonamides; D000077484:Vemurafenib