KRASG12D- and BRAFV600E-Induced Transformation of Murine Pancreatic Epithelial Cells Requires MEK/ERK-Stimulated IGF1R Signaling
Appleman V, Ahronian L, Cai J, Klimstra D, Lewis B. KRASG12D- and BRAFV600E-Induced Transformation of Murine Pancreatic Epithelial Cells Requires MEK/ERK-Stimulated IGF1R Signaling. Molecular Cancer Research 2012, 10: 1228-1239. PMID: 22871572, PMCID: PMC3973739, DOI: 10.1158/1541-7786.mcr-12-0340-t.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCarcinogenesisCarcinoma, Pancreatic DuctalCell ProliferationCell SurvivalDisease Models, AnimalEpithelial CellsGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansMAP Kinase Signaling SystemMiceMice, NudeMice, TransgenicMitogen-Activated Protein Kinase KinasesMutation, MissensePancreasPancreatic NeoplasmsPhosphatidylinositol 3-KinasesPhosphorylationProto-Oncogene Proteins B-rafProto-Oncogene Proteins c-aktProto-Oncogene Proteins p21(ras)Receptor, IGF Type 1Recombinant Fusion ProteinsConceptsPancreatic ductal adenocarcinomaPancreatic ductal epithelial cellsMAP-ERK kinaseIGF1R signalingInsulin-like growth factor (IGF) receptorsPancreatic tumor initiationInhibition of MAP-ERK kinaseExposure to apoptotic stimuliPI3K/Akt signalingMutations of KRASPutative cell of originDuctal epithelial cellsCell of originCells to apoptosisActivation of PI3K/Akt signalingOrthotopic modelMEK inhibitionDuctal adenocarcinomaAutocrine activationPutative cellTumor initiationTherapeutic strategiesTumor formationEpithelial cellsIncreased Survival
This site is protected by hCaptcha and its Privacy Policy and Terms of Service apply