2024
Overexpression of Malat1 drives metastasis through inflammatory reprogramming of the tumor microenvironment
Martinez-Terroba E, Plasek-Hegde L, Chiotakakos I, Li V, de Miguel F, Robles-Oteiza C, Tyagi A, Politi K, Zamudio J, Dimitrova N. Overexpression of Malat1 drives metastasis through inflammatory reprogramming of the tumor microenvironment. Science Immunology 2024, 9: eadh5462. PMID: 38875320, DOI: 10.1126/sciimmunol.adh5462.Peer-Reviewed Original ResearchConceptsTumor microenvironmentLung adenocarcinomaMetastatic diseasePromoting metastatic diseaseGlobal chromatin accessibilityMetastasis-associated lung adenocarcinoma transcript 1Overexpression of MALAT1Lung adenocarcinoma transcript 1Lung adenocarcinoma metastasisCCL2 blockadeInflammatory reprogrammingEnhanced cell mobilityMacrophage depletionMechanism of actionTumor typesTumor progressionMouse modelCell mobilizationTumorLong noncoding RNAsParacrine secretionMetastasisCell linesTranscript 1Microenvironment
2018
The Impact of Smoking and TP53 Mutations in Lung Adenocarcinoma Patients with Targetable Mutations—The Lung Cancer Mutation Consortium (LCMC2)
Aisner DL, investigators F, Sholl L, Berry L, Rossi M, Chen H, Fujimoto J, Moreira A, Ramalingam S, Villaruz L, Otterson G, Haura E, Politi K, Glisson B, Cetnar J, Garon E, Schiller J, Waqar S, Sequist L, Brahmer J, Shyr Y, Kugler K, Wistuba I, Johnson B, Minna J, Kris M, Bunn P, Kwiatkowski D. The Impact of Smoking and TP53 Mutations in Lung Adenocarcinoma Patients with Targetable Mutations—The Lung Cancer Mutation Consortium (LCMC2). Clinical Cancer Research 2018, 24: 1038-1047. PMID: 29217530, PMCID: PMC7008001, DOI: 10.1158/1078-0432.ccr-17-2289.Peer-Reviewed Original ResearchMeSH KeywordsAdenocarcinoma of LungAdultAgedAged, 80 and overAntineoplastic AgentsBiomarkers, TumorCarcinogenesisDNA Mutational AnalysisFemaleHigh-Throughput Nucleotide SequencingHumansLung NeoplasmsMaleMiddle AgedMolecular Targeted TherapyMutationPrognosisProspective StudiesSmokingSurvival AnalysisTreatment OutcomeTumor Suppressor Protein p53Young AdultConceptsLung Cancer Mutation ConsortiumLung adenocarcinomaPrior smoking historyTargetable driver alterationsSimilar survival benefitAdvanced lung adenocarcinomaHistory of smokingOncogenic driver mutationsEfficacy of treatmentClin Cancer ResClinical characteristicsSmoking historySurvival benefitShorter survivalTargetable driversLung cancerPredictive markerLonger survivalOncogenic driver eventsTargeted therapyTherapy selectionCancer-related genesPatientsDriver alterationsMolecular testing
2012
Targeting the FOXO1/KLF6 axis regulates EGFR signaling and treatment response
Sangodkar J, Dhawan N, Melville H, Singh V, Yuan E, Rana H, Izadmehr S, Farrington C, Mazhar S, Katz S, Albano T, Arnovitz P, Okrent R, Ohlmeyer M, Galsky M, Burstein D, Zhang D, Politi K, DiFeo A, Narla G. Targeting the FOXO1/KLF6 axis regulates EGFR signaling and treatment response. Journal Of Clinical Investigation 2012, 122: 2637-2651. PMID: 22653055, PMCID: PMC3386822, DOI: 10.1172/jci62058.Peer-Reviewed Original ResearchMeSH KeywordsActive Transport, Cell NucleusAdenocarcinomaAdenocarcinoma of LungAnimalsAntineoplastic AgentsCell Line, TumorDrug Resistance, NeoplasmDrug SynergismEnzyme ActivationErbB ReceptorsErlotinib HydrochlorideFemaleForkhead Box Protein O1Forkhead Transcription FactorsGene Expression Regulation, NeoplasticHumansKruppel-Like Factor 6Kruppel-Like Transcription FactorsLung NeoplasmsMiceMice, Inbred BALB CMice, NudeMutationProto-Oncogene ProteinsProto-Oncogene Proteins c-aktQuinazolinesReal-Time Polymerase Chain ReactionSignal TransductionTranscription, GeneticTrifluoperazineTumor BurdenXenograft Model Antitumor AssaysConceptsAnti-EGFR-based therapyEGFR signalingKruppel-like factor 6Lung adenocarcinomaForkhead box O1Xenograft models of lung adenocarcinomaModel of lung adenocarcinomaMetastatic lung adenocarcinomaTreat advanced cancersMolecular drivers of disease progressionDrivers of disease progressionOncogenic EGFR signalingActivation of Akt signalingFoxO1 nuclear exportTreating resistant diseaseIn vivo modelsCell culturesErlotinib resistanceResistant diseaseTreatment responseMolecular therapiesXenograft modelFDA-approved drugsDisease progressionEGFR activation