2016
Oncogenic EGFR Represses the TET1 DNA Demethylase to Induce Silencing of Tumor Suppressors in Cancer Cells
Forloni M, Gupta R, Nagarajan A, Sun LS, Dong Y, Pirazzoli V, Toki M, Wurtz A, Melnick MA, Kobayashi S, Homer RJ, Rimm DL, Gettinger SJ, Politi K, Dogra SK, Wajapeyee N. Oncogenic EGFR Represses the TET1 DNA Demethylase to Induce Silencing of Tumor Suppressors in Cancer Cells. Cell Reports 2016, 16: 457-471. PMID: 27346347, PMCID: PMC4945411, DOI: 10.1016/j.celrep.2016.05.087.Peer-Reviewed Original ResearchMeSH KeywordsAdenocarcinomaAdenocarcinoma of LungAntineoplastic AgentsBrain NeoplasmsCCAAT-Enhancer-Binding ProteinsCell Line, TumorCpG IslandsDNA MethylationDrug Screening Assays, AntitumorErbB ReceptorsGene Expression Regulation, NeoplasticGene SilencingGlioblastomaHumansLung NeoplasmsMAP Kinase Signaling SystemMixed Function OxygenasesMutationOncogenesProtein Kinase InhibitorsProto-Oncogene ProteinsTranscription, GeneticTumor Suppressor ProteinsUp-RegulationConceptsOncogenic epidermal growth factor receptorMethylation-mediated transcriptional silencingEpidermal growth factor receptorTumor suppressorTranscriptional silencingActive DNA demethylationCancer cellsFamily member 1TET1 knockdownDNA demethylaseDNA demethylationTranscription factorsGrowth factor receptorEctopic expressionCytoplasmic localizationGlioblastoma tumor growthLung cancer cellsTET1 expressionFunctional roleSuppressorFactor receptorMember 1TET1SilencingLung cancer samples
2015
Conditional overexpression of TGFβ1 promotes pulmonary inflammation, apoptosis and mortality via TGFβR2 in the developing mouse lung
Sureshbabu A, Syed MA, Boddupalli CS, Dhodapkar MV, Homer RJ, Minoo P, Bhandari V. Conditional overexpression of TGFβ1 promotes pulmonary inflammation, apoptosis and mortality via TGFβR2 in the developing mouse lung. Respiratory Research 2015, 16: 4. PMID: 25591994, PMCID: PMC4307226, DOI: 10.1186/s12931-014-0162-6.Peer-Reviewed Original ResearchMeSH KeywordsAcute Lung InjuryAlveolar Epithelial CellsAnimalsAnimals, NewbornApoptosisDisease Models, AnimalGenotypeHumansHyperoxiaLungMice, Inbred C57BLMice, KnockoutMice, TransgenicPhenotypePneumoniaProtein Serine-Threonine KinasesReceptor, Transforming Growth Factor-beta Type IIReceptors, Transforming Growth Factor betaSignal TransductionTime FactorsTransforming Growth Factor beta1Up-RegulationConceptsImpaired alveolarizationBronchopulmonary dysplasiaAlveolar epithelial cellsPulmonary inflammationPulmonary phenotypeMouse lungAcute lung injuryType II alveolar epithelial cellsApoptotic cell deathCell deathNewborn mouse lungPotential therapeutic strategyGrowth factor betaNull mutant miceLung injuryImproved survivalNeonatal mortalityMonocyte infiltrationAbnormal alveolarizationAngiogenic mediatorsInflammatory signalsTGFβ1 expressionTherapeutic strategiesInflammatory macrophagesLung morphometry
2010
High expression of BCL-2 predicts favorable outcome in non-small cell lung cancer patients with non squamous histology
Anagnostou VK, Lowery FJ, Zolota V, Tzelepi V, Gopinath A, Liceaga C, Panagopoulos N, Frangia K, Tanoue L, Boffa D, Gettinger S, Detterbeck F, Homer RJ, Dougenis D, Rimm DL, Syrigos KN. High expression of BCL-2 predicts favorable outcome in non-small cell lung cancer patients with non squamous histology. BMC Cancer 2010, 10: 186. PMID: 20459695, PMCID: PMC2875218, DOI: 10.1186/1471-2407-10-186.Peer-Reviewed Original ResearchMeSH KeywordsAdenocarcinomaAgedBiomarkers, TumorCarcinoma, Large CellCarcinoma, Non-Small-Cell LungCarcinoma, Squamous CellCell DifferentiationCohort StudiesConnecticutFemaleGreeceHumansKaplan-Meier EstimateLung NeoplasmsMaleMiddle AgedNeoplasm StagingPredictive Value of TestsProportional Hazards ModelsProto-Oncogene Proteins c-bcl-2Reproducibility of ResultsRetrospective StudiesRisk AssessmentRisk FactorsTime FactorsTreatment OutcomeUp-RegulationConceptsNon-small cell lung cancer patientsCell lung cancer patientsNon-squamous tumorsLung cancer patientsBcl-2 expressionNSCLC patientsCancer patientsBcl-2Favorable outcomeIndependent cohortSmall cell lung cancer patientsIndependent lower riskNon-squamous histologySubgroup of patientsHigh expressersSquamous cell carcinomaHigh Bcl-2 expressionBcl-2 protein levelsSquamous histologyMedian survivalPrognostic factorsValidation cohortCell carcinomaPathological characteristicsPrognostic stratification
2004
Acidic Mammalian Chitinase in Asthmatic Th2 Inflammation and IL-13 Pathway Activation
Zhu Z, Zheng T, Homer RJ, Kim YK, Chen NY, Cohn L, Hamid Q, Elias JA. Acidic Mammalian Chitinase in Asthmatic Th2 Inflammation and IL-13 Pathway Activation. Science 2004, 304: 1678-1682. PMID: 15192232, DOI: 10.1126/science.1095336.Peer-Reviewed Original ResearchConceptsTh2 inflammationAcidic mammalian chitinaseIL-13-induced responsesPathway activationTh2-dominated disordersMammalian chitinaseAirway hyperresponsivenessAsthma modelT helperHuman asthmaChemokine inductionInterleukin-13Exaggerated quantitiesImportant mediatorEpithelial cellsAsthmaInflammationActivationHyperresponsivenessInfectionThe C10/CCL6 Chemokine and CCR1 Play Critical Roles in the Pathogenesis of IL-13-Induced Inflammation and Remodeling
Ma B, Zhu Z, Homer RJ, Gerard C, Strieter R, Elias JA. The C10/CCL6 Chemokine and CCR1 Play Critical Roles in the Pathogenesis of IL-13-Induced Inflammation and Remodeling. The Journal Of Immunology 2004, 172: 1872-1881. PMID: 14734772, DOI: 10.4049/jimmunol.172.3.1872.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCathepsinsChemokine CCL2Chemokines, CCDown-RegulationImmune SeraInflammationInterleukin-13LungLung ComplianceLung Volume MeasurementsMatrix Metalloproteinase 2Matrix Metalloproteinase 9MiceMice, Inbred C57BLMice, KnockoutMice, TransgenicProtease InhibitorsPulmonary AlveoliReceptors, CCR1Receptors, ChemokineUp-RegulationConceptsIL-13-induced inflammationMatrix metalloproteinase-2IL-13Potent stimulatorMMP-9Alveolar remodelingMonocyte chemoattractant protein-1Transgenic IL-13Inflammatory protein-1alphaChemoattractant protein-1Wild-type miceIL-13 stimulationPulmonary phenotypeLevels of mRNAMetalloproteinase-4Murine lungMetalloproteinase-2Tissue inhibitorInflammationTargeted null mutationCompliance alterationsPathogenesisCCL6ChemokinesProtein 1
2001
IL-4 Promotes Airway Eosinophilia by Suppressing IFN-γ Production: Defining a Novel Role for IFN-γ in the Regulation of Allergic Airway Inflammation
Cohn L, Herrick C, Niu N, Homer R, Bottomly K. IL-4 Promotes Airway Eosinophilia by Suppressing IFN-γ Production: Defining a Novel Role for IFN-γ in the Regulation of Allergic Airway Inflammation. The Journal Of Immunology 2001, 166: 2760-2767. PMID: 11160342, DOI: 10.4049/jimmunol.166.4.2760.Peer-Reviewed Original ResearchMeSH KeywordsAdministration, CutaneousAdministration, IntranasalAdoptive TransferAnimalsBone Marrow CellsBone Marrow TransplantationBronchiCell MovementDown-RegulationEosinophilsFemaleHematopoietic Stem CellsInflammationInterferon-gammaInterleukin-13Interleukin-4Interleukin-5MaleMiceMice, Inbred BALB CMice, KnockoutMice, TransgenicOvalbuminPulmonary EosinophiliaReceptors, InterferonRespiratory HypersensitivityTh2 CellsUp-RegulationConceptsAirway eosinophiliaIL-4IFN-gammaTh2 cellsAirway eosinophilsIL-5Allergic airway inflammationIFN-γ productionTh2 cell generationAirway inflammationEosinophilic inflammationLung eosinophiliaLung parenchymalTh2 cytokinesIntranasal administrationRespiratory tractLung tissueCounterregulatory effectsEosinophiliaCell transferEosinophilsHemopoietic cellsInflammationAirwayIFN