2019
Loss of thymidine kinase 1 inhibits lung cancer growth and metastatic attributes by reducing GDF15 expression
Malvi P, Janostiak R, Nagarajan A, Cai G, Wajapeyee N. Loss of thymidine kinase 1 inhibits lung cancer growth and metastatic attributes by reducing GDF15 expression. PLOS Genetics 2019, 15: e1008439. PMID: 31589613, PMCID: PMC6797230, DOI: 10.1371/journal.pgen.1008439.Peer-Reviewed Original ResearchMeSH KeywordsAdenocarcinoma of LungAdultAgedAnimalsBiomarkers, TumorCell Line, TumorCell MovementCell ProliferationDatasets as TopicDNA-Binding ProteinsFemaleGene Expression Regulation, NeoplasticGene Knockdown TechniquesGrowth Differentiation Factor 15HumansLungLung NeoplasmsMaleMiceMiddle AgedNeoplasm Recurrence, LocalPrognosisSurvival AnalysisThymidine KinaseTranscription FactorsXenograft Model Antitumor AssaysConceptsShort hairpin RNALUAD cellsMetastatic attributesRho GTPase activityMAP kinase pathwayEctopic expressionGTPase activityTranscriptional overexpressionKinase pathwayKinase 1Cancer cell growthGenetic knockdownProfiling-based approachDifferentiation factor 15Hairpin RNALung adenocarcinoma patientsLung cancer growthCell growthLUAD therapyDownstream mediatorLUAD tumorsLUAD growthKey hallmarksReduced expressionDependent manner
2014
Acquired Resistance of EGFR-Mutant Lung Adenocarcinomas to Afatinib plus Cetuximab Is Associated with Activation of mTORC1
Pirazzoli V, Nebhan C, Song X, Wurtz A, Walther Z, Cai G, Zhao Z, Jia P, de Stanchina E, Shapiro EM, Gale M, Yin R, Horn L, Carbone DP, Stephens PJ, Miller V, Gettinger S, Pao W, Politi K. Acquired Resistance of EGFR-Mutant Lung Adenocarcinomas to Afatinib plus Cetuximab Is Associated with Activation of mTORC1. Cell Reports 2014, 7: 999-1008. PMID: 24813888, PMCID: PMC4074596, DOI: 10.1016/j.celrep.2014.04.014.Peer-Reviewed Original ResearchMeSH KeywordsAdenocarcinomaAdenocarcinoma of LungAfatinibAnimalsAntibodies, Monoclonal, HumanizedAntineoplastic Combined Chemotherapy ProtocolsCell Line, TumorCetuximabDrug Resistance, NeoplasmErbB ReceptorsHumansLung NeoplasmsMechanistic Target of Rapamycin Complex 1MiceMice, NudeMice, TransgenicMultiprotein ComplexesMutationQuinazolinesRandom AllocationTOR Serine-Threonine KinasesXenograft Model Antitumor AssaysConceptsTyrosine kinase inhibitorsFirst-generation tyrosine kinase inhibitorEGFR-mutant lung adenocarcinomaLung adenocarcinomaMechanisms of resistanceEGFR antibody cetuximabPotential therapeutic strategyBiopsy specimensAntibody cetuximabDrug combinationsMouse modelTherapeutic strategiesAfatinibAddition of rapamycinCetuximabDual inhibitionAcquired ResistanceKinase inhibitorsGenomic alterationsAdenocarcinomaPatientsActivationGenomic mechanismsDrugsMTORC1 activation