2023
Efficacy of Osimertinib in Patients with Lung Cancer Positive for Uncommon EGFR Exon 19 Deletion Mutations
Grant M, Aredo J, Starrett J, Stockhammer P, van Rosenburgh I, Wurtz A, Piper-Valillo A, Piotrowska Z, Falcon C, Yu H, Aggarwal C, Scholes D, Patil T, Nguyen C, Phadke M, Li F, Neal J, Lemmon M, Walther Z, Politi K, Goldberg S. Efficacy of Osimertinib in Patients with Lung Cancer Positive for Uncommon EGFR Exon 19 Deletion Mutations. Clinical Cancer Research 2023, 29: of1-of8. PMID: 36913537, PMCID: PMC10493186, DOI: 10.1158/1078-0432.ccr-22-3497.Peer-Reviewed Original ResearchConceptsProgression-free survivalNon-small cell lung cancerInferior progression-free survivalMulticenter retrospective cohortEfficacy of osimertinibMulti-institutional cohortCell lung cancerExon 19 deletion mutationUncommon EGFRRetrospective cohortClinical outcomesClinical efficacyLung cancerOsimertinib efficacyEGFR mutationsPreclinical modelsEx19delPatientsAACR Genie databaseLater linesOsimertinibMutant cohortFirst lineCohortEfficacy
2021
HDAC Inhibition Induces Cell Cycle Arrest and Mesenchymal-Epithelial Transition in a Novel Pleural-Effusion Derived Uterine Carcinosarcoma Cell Line
Stockhammer P, Okumus Ö, Hegedus L, Rittler D, Ploenes T, Herold T, Kalbourtzis S, Bankfalvi A, Sucker A, Kimmig R, Aigner C, Hegedus B. HDAC Inhibition Induces Cell Cycle Arrest and Mesenchymal-Epithelial Transition in a Novel Pleural-Effusion Derived Uterine Carcinosarcoma Cell Line. Pathology & Oncology Research 2021, 27: 636088. PMID: 34257602, PMCID: PMC8262245, DOI: 10.3389/pore.2021.636088.Peer-Reviewed Original ResearchMeSH KeywordsAntineoplastic Combined Chemotherapy ProtocolsBiomarkers, TumorCarcinosarcomaCell Cycle CheckpointsCisplatinEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHistone DeacetylasesHumansMiddle AgedMutationPaclitaxelPhthalazinesPiperazinesPleural Effusion, MalignantPrognosisPyrazolesQuinolinesTumor Cells, CulturedUterine NeoplasmsVorinostatConceptsEpithelial-mesenchymal transitionUterine carcinosarcomaPleural effusionMesenchymal-epithelial transitionCell linesPatient-derived preclinical modelsMalignant pleural effusionMetastatic tumor lesionsVimentin-positive tumorsE-cadherinCarcinosarcoma cell lineInduces cell cycle arrestHistone deacetylase inhibitionFirst-line chemotherapeuticsΒ-catenin expressionE-cadherin expressionPSmad2 expressionCell cycle analysisPositive tumorsAggressive malignancyMetastatic tumorsDisease progressionCell cycle arrestNovel therapiesPreclinical models
2020
Telomerase Reverse Transcriptase Promoter Mutations Identify a Genomically Defined and Highly Aggressive Human Pleural Mesothelioma Subgroup
Pirker C, Bilecz A, Grusch M, Mohr T, Heidenreich B, Laszlo V, Stockhammer P, Lötsch-Gojo D, Gojo J, Gabler L, Spiegl-Kreinecker S, Dome B, Steindl A, Klikovits T, Hoda MA, Jakopovic M, Samarzija M, Mohorcic K, Kern I, Kiesel B, Brcic L, Oberndorfer F, Müllauer L, Klepetko W, Schmidt WM, Kumar R, Hegedus B, Berger W. Telomerase Reverse Transcriptase Promoter Mutations Identify a Genomically Defined and Highly Aggressive Human Pleural Mesothelioma Subgroup. Clinical Cancer Research 2020, 26: 3819-3830. PMID: 32317288, DOI: 10.1158/1078-0432.ccr-19-3573.Peer-Reviewed Original ResearchMeSH KeywordsAgedBiomarkers, TumorCell Line, TumorCell SurvivalCell Transformation, NeoplasticComparative Genomic HybridizationDisease ProgressionDNA Mutational AnalysisExome SequencingFemaleGene Expression ProfilingHumansKaplan-Meier EstimateMaleMesothelioma, MalignantMiddle AgedMutationPleuraPleural NeoplasmsPrognosisPromoter Regions, GeneticRetrospective StudiesTelomeraseConceptsHuman malignant pleural mesotheliomaMalignant pleural mesotheliomaPromoter mutationsLuciferase promoter assaysGene expression profilingImmortalized cell linesArray comparative genomic hybridizationComparative genomic hybridizationWild-type samplesGene promoterExpression profilingPromoter assaysPromoter activityTelomerase reverse transcriptase gene promoterCell immortalizationMolecular mechanismsMutations/deletionsMalignant transformation processMPM casesSpecific mutation patternsGenomic hybridizationTelomerase activityGenomic alteration patternsMutationsChromosomal alterationsHDAC inhibition synergizes with ALK inhibitors to overcome resistance in a novel ALK mutated lung adenocarcinoma model
Stockhammer P, Ho CSL, Hegedus L, Lotz G, Molnár E, Bankfalvi A, Herold T, Kalbourtzis S, Ploenes T, Eberhardt WEE, Schuler M, Aigner C, Schramm A, Hegedus B. HDAC inhibition synergizes with ALK inhibitors to overcome resistance in a novel ALK mutated lung adenocarcinoma model. Lung Cancer 2020, 144: 20-29. PMID: 32353632, DOI: 10.1016/j.lungcan.2020.04.002.Peer-Reviewed Original ResearchConceptsALK tyrosine kinase inhibitorsCell linesALK fusion oncogeneDistinct resistance mutationsTreatment-naïve ALKMalignant pleural effusionPost-treatment tumorsLung cancer modelPan-HDAC inhibitorsNovel therapeutic approachesTyrosine kinase inhibitorsMesenchymal transition (EMT) markersLung adenocarcinoma modelTime of resistancePleural effusionALK inhibitionLung adenocarcinomaSubcutaneous xenograftsALK inhibitorsTherapeutic approachesCell line pairsCancer modelAdenocarcinoma modelHDAC inhibitionTransition markers