Paul Stockhammer, MD, PhD
About
Research
Publications
2024
Comprehensive characterization of ERBB2 genomic alterations inlung cancer.
El Zarif T, Stockhammer P, Schillo J, Goldberg S, Politi K, Grant M. Comprehensive characterization of ERBB2 genomic alterations inlung cancer. Journal Of Clinical Oncology 2024, 42: 3148-3148. DOI: 10.1200/jco.2024.42.16_suppl.3148.Peer-Reviewed Original ResearchNon-small cell lung cancerProgression-free survivalShorter progression-free survivalTyrosine kinase domainSystemic therapyCo-mutationsClinical characteristics of non-small cell lung cancerCharacteristics of non-small cell lung cancerFirst-line platinum-based chemotherapyMedian tumor mutation burdenNon-small cell lung cancer tumorsFirst-line systemic therapyTP53 co-mutationsPlatinum-based chemotherapyTumor mutational burdenKaplan-Meier methodCell lung cancerLog-rank testOptimal treatment strategyHistory of smokingCopy number profilesTumor profile dataJuxtamembrane domainSquamous histologyTrastuzumab deruxtecanERBB2 mutations and association with molecular phenotype in urothelial carcinoma.
Zarif T, Stockhammer P, Semaan K, Eid M, Chehade R, Nawfal R, Yekeduz E, Nassar A, Lee G, Baca S, CHOUEIRI T, Grant M, Bellmunt J. ERBB2 mutations and association with molecular phenotype in urothelial carcinoma. Journal Of Clinical Oncology 2024, 42: 4590-4590. DOI: 10.1200/jco.2024.42.16_suppl.4590.Peer-Reviewed Original ResearchUpper tract UCTumor mutational burdenUrothelial carcinomaERBB2-targeted therapyMutant tumorsUC tumorsERBB2 amplificationMedian tumor mutation burdenHigh tumor mutational burdenWild type tumorsChi-square and Mann-Whitney U testsCombination therapy studiesMolecular phenotypesMann-Whitney U testTumor profile dataERBB2 mutationsBladder UCPolyPhen-2Mutational burdenType tumorsGenomic dataSolid tumorsClinical characteristicsCo-mutationsActivating mutations
2023
Krebs von den Lungen 6 (KL-6) is a novel diagnostic and prognostic biomarker in pleural mesothelioma
Stockhammer P, Baumeister H, Ploenes T, Bonella F, Theegarten D, Dome B, Pirker C, Berger W, Hegedüs L, Baranyi M, Schuler M, Deshayes S, Bölükbas S, Aigner C, Blanquart C, Hegedüs B. Krebs von den Lungen 6 (KL-6) is a novel diagnostic and prognostic biomarker in pleural mesothelioma. Lung Cancer 2023, 185: 107360. PMID: 37713954, DOI: 10.1016/j.lungcan.2023.107360.Peer-Reviewed Original ResearchKrebs von den Lungen-6KL-6 levelsPleural mesotheliomaIndependent validation cohortPM patientsPrognostic biomarkerLungen-6Overall survivalValidation cohortPrimary cell linesHigher KL-6 levelsLower KL-6 levelsChemiluminescence enzyme immunoassayPleural effusion levelsSystemic treatment optionsBetter overall survivalNon-malignant controlsPleural effusion samplesCell line supernatantsMucin-1 glycoproteinCell linesMUC1 mRNA expressionEffusion levelsPleural disordersConsecutive patientsEfficacy 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 lineCohortEfficacyKL-6 is a potential diagnostic biomarker for pleural mesothelioma
Schulten H, Stockhammer P, Bonella F, Plönes T, Aigner C, Hegedüs B. KL-6 is a potential diagnostic biomarker for pleural mesothelioma. Pneumologie 2023, 77: s106-s107. DOI: 10.1055/s-0043-1761130.Peer-Reviewed Original Research
2022
Explorative Analyse zirkulierende Biomarker bei malignen Pleuraergüssen extrapulmonaler Primärtumore
Koziej P, Okumus Ö, Stockhammer P, Plönes T, Collaud S, Hegedüs B, Aigner C. Explorative Analyse zirkulierende Biomarker bei malignen Pleuraergüssen extrapulmonaler Primärtumore. Zentralblatt Für Chirurgie - Zeitschrift Für Allgemeine Viszeral- Thorax- Und Gefäßchirurgie 2022, 147: s66-s66. DOI: 10.1055/s-0042-1754234.Peer-Reviewed Original Research
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
Multicellular contractility contributes to the emergence of mesothelioma nodules
Tarnoki-Zach J, Stockhammer P, Isai DG, Mehes E, Szeder B, Kovacs I, Bugyik E, Paku S, Berger W, Thomas SM, Neufeld Z, Dome B, Hegedus B, Czirok A. Multicellular contractility contributes to the emergence of mesothelioma nodules. Scientific Reports 2020, 10: 20114. PMID: 33208866, PMCID: PMC7675981, DOI: 10.1038/s41598-020-76641-x.Peer-Reviewed Original ResearchTelomerase 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 Induces PD-L1 Expression in a Novel Anaplastic Thyroid Cancer Cell Line
Hegedűs L, Rittler D, Garay T, Stockhammer P, Kovács I, Döme B, Theurer S, Hager T, Herold T, Kalbourtzis S, Bankfalvi A, Schmid KW, Führer D, Aigner C, Hegedűs B. HDAC Inhibition Induces PD-L1 Expression in a Novel Anaplastic Thyroid Cancer Cell Line. Pathology & Oncology Research 2020, 26: 2523-2535. PMID: 32591993, PMCID: PMC7471186, DOI: 10.1007/s12253-020-00834-y.Peer-Reviewed Original ResearchConceptsPD-L1 expressionAnaplastic thyroid cancerPapillary thyroid cancerHDAC inhibitor treatmentThyroid cancerInhibitor treatmentHDAC inhibitionAdditional preclinical modelsAnaplastic thyroid cancer cell linesAnaplastic thyroid cancer cellsMalignant pleural effusionThyroid cancer cell linesNew therapeutic optionsThyroid cancer cellsCell linesCancer cell linesStandard chemotherapyFavorable prognosisMale patientsClinical outcomesNovel cell linePleural effusionTherapeutic optionsAggressive malignancyCell cycle arrest