Development of New Mouse Lung Tumor Models Expressing EGFR T790M Mutants Associated with Clinical Resistance to Kinase Inhibitors 英文参考文献.docVIP

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Development of New Mouse Lung Tumor Models Expressing EGFR T790M Mutants Associated with Clinical Resistance to Kinase Inhibitors 英文参考文献.doc

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Development of New Mouse Lung Tumor Models Expressing EGFR T790M Mutants Associated with Clinical Resistance to Kinase Inhibitors 英文参考文献

DevelopmentofNewMouseLungTumorModels ExpressingEGFRT790MMutantsAssociatedwithClinical ResistancetoKinaseInhibitors LuciaRegales1,MarissaN.Balak1,YixuanGong1,KaterinaPoliti2,AyanaSawai3,CarlLe4,JasonA.Koutcher4,DavidB.Solit5,NealRosen3, MaureenF.Zakowski6,WilliamPao1,7* 1PaoLab,HumanOncologyandPathogenesisProgram,MemorialSloan-KetteringCancerCenter,NewYork,NewYork,UnitedStatesofAmerica, 2VarmusLab,CancerBiologyandGeneticsProgram,MemorialSloan-KetteringCancerCenter,NewYork,NewYork,UnitedStatesofAmerica,3Rosen Lab, Molecular Pharmacology and Chemistry Program, Memorial Sloan-Kettering Cancer Center, New York, New York, United States of America, 4ImagingandSpectroscopicPhysicsService,DepartmentofMedicalPhysics,MemorialSloan-KetteringCancerCenter,NewYork,NewYork,United StatesofAmerica,5SolitLab,HumanOncologyandPathogenesisProgram,MemorialSloan-KetteringCancerCenter,NewYork,NewYork,United States of America, 6Department of Pathology, Memorial Sloan-Kettering Cancer Center, New York, New York, United States of America, 77 DepartmentofMedicine,WeillMedicalCollegeofCornellUniversity,NewYork,NewYork,UnitedStatesofAmerica Background. The EGFR T790M mutation confers acquired resistance to kinase inhibitors in human EGFR mutant lung adenocarcinoma, is occasionally detected before treatment, and may confer genetic susceptibility to lung cancer. Methodology/Principal Findings. To study further its role in lung tumorigenesis, we developed mice with inducible expressionintypeIIpneumocytesofEGFRT790Maloneortogetherwithadrug-sensitiveL858Rmutation.Bothtransgeniclines developlungadenocarcinomasthatrequiremutantEGFRfortumormaintenancebutareresistanttoanEGFRkinaseinhibitor. L858R+T790M EGFR -driven tumors are transiently targeted by hsp90 inhibition. Notably, EGFRT790M-expressing animals develop tumors with longer latency than EGFRL858R+T790M-bearing mice and in the absence of additional kinase domain mutations. Conclusions/Significance.ThesenewmousemodelsofmutantEGFR-dependentlungade