title: RAF/MEK dependence of KRAS-mutant pancreatic ductal adenocarcinomas.
abstract: Studies using genetically engineered mouse models indicate that RAF activation is sufficient to induce pancreatic intraepithelial neoplasms, suggesting that mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK) kinase (MEK) inhibitor-based combination approaches may have clinical use in patients with pancreatic ductal adenocarcinomas.
authors.affiliation: Human Oncology and Pathogenesis Program, Memorial Sloan-Kettering Cancer Center, New York, USA.
authors.forename: Aphrothiti J
authors.initials: AJ
authors.lastname: Hanrahan
authors.forename: David B
authors.initials: DB
authors.lastname: Solit
mesh_terms: D000818:Animals; D021441:Carcinoma, Pancreatic Ductal / Q000201:enzymology*; D002471:Cell Transformation, Neoplastic / Q000378:metabolism*; D048049:Extracellular Signal-Regulated MAP Kinases / Q000378:metabolism*; D006801:Humans; D020935:MAP Kinase Signaling System; D020929:Mitogen-Activated Protein Kinase Kinases / Q000378:metabolism*; D010190:Pancreatic Neoplasms / Q000201:enzymology*; D048493:Proto-Oncogene Proteins B-raf / Q000378:metabolism*
chemical_list: C482119:BRAF protein, human; D048493:Proto-Oncogene Proteins B-raf; D048049:Extracellular Signal-Regulated MAP Kinases; D020929:Mitogen-Activated Protein Kinase Kinases