2018
Concomitant targeting of the mTOR/MAPK pathways: novel therapeutic strategy in subsets of RICTOR/KRAS-altered non-small cell lung cancer
Ruder D, Papadimitrakopoulou V, Shien K, Behrens C, Kalhor N, Chen H, Shen L, Lee JJ, Hong WK, Tang X, Girard L, Minna JD, Diao L, Wang J, Mino B, Villalobos P, Rodriguez-Canales J, Hanson NE, Sun J, Miller V, Greenbowe J, Frampton G, Herbst RS, Baladandayuthapani V, Wistuba II, Izzo JG. Concomitant targeting of the mTOR/MAPK pathways: novel therapeutic strategy in subsets of RICTOR/KRAS-altered non-small cell lung cancer. Oncotarget 2018, 9: 33995-34008. PMID: 30338041, PMCID: PMC6188056, DOI: 10.18632/oncotarget.26129.Peer-Reviewed Original ResearchLung cancerAdvanced non-small cell lung cancer (NSCLC) patientsNon-small cell lung cancer patientsNon-small cell lung cancerCell lung cancer patientsSubset of NSCLCWorse overall survivalCell lung cancerLung cancer patientsAnti-tumor effectsNovel therapeutic strategiesNSCLC cell linesTherapeutic paradigm shiftMAPK pathwayUnique therapeutic vulnerabilitiesOverall survivalCancer patientsClinical trialsLung adenocarcinomaKRAS/Therapeutic strategiesPharmacologic inhibitionTherapeutic vulnerabilitiesTherapeutic opportunitiesConcomitant targeting
2015
Co-occurring Genomic Alterations Define Major Subsets of KRAS-Mutant Lung Adenocarcinoma with Distinct Biology, Immune Profiles, and Therapeutic Vulnerabilities
Skoulidis F, Byers LA, Diao L, Papadimitrakopoulou VA, Tong P, Izzo J, Behrens C, Kadara H, Parra ER, Canales JR, Zhang J, Giri U, Gudikote J, Cortez MA, Yang C, Fan Y, Peyton M, Girard L, Coombes KR, Toniatti C, Heffernan TP, Choi M, Frampton GM, Miller V, Weinstein JN, Herbst RS, Wong KK, Zhang J, Sharma P, Mills GB, Hong WK, Minna JD, Allison JP, Futreal A, Wang J, Wistuba II, Heymach JV. Co-occurring Genomic Alterations Define Major Subsets of KRAS-Mutant Lung Adenocarcinoma with Distinct Biology, Immune Profiles, and Therapeutic Vulnerabilities. Cancer Discovery 2015, 5: 860-877. PMID: 26069186, PMCID: PMC4527963, DOI: 10.1158/2159-8290.cd-14-1236.Peer-Reviewed Original ResearchMeSH KeywordsAdenocarcinomaAdenocarcinoma of LungAMP-Activated Protein Kinase KinasesAMP-Activated Protein KinasesCell Line, TumorCluster AnalysisDNA-Binding ProteinsGene ExpressionGene Expression ProfilingGenetic VariationGenomicsHumansInflammationLung NeoplasmsMutationOxidative StressPrognosisProtein Serine-Threonine KinasesRas ProteinsSignal TransductionTranscription FactorsTumor Suppressor ProteinsConceptsKRAS-mutant lung adenocarcinomaCo-occurring genomic alterationsLung adenocarcinomaDistinct biologyTherapeutic vulnerabilitiesSTK11/LKB1Hsp90 inhibitor therapyRelapse-free survivalDrug sensitivity patternsGenomic alterationsCDKN2A/BKC tumorsInflammatory markersMucinous histologyImmune markersImmune profilePD-L1AdenocarcinomaSensitivity patternMajor subsetNKX2-1 transcription factorLow expressionTumorsGenetic alterationsEffector molecules