Paul Stockhammer, MD, PhD
Clinical FellowAbout
Research
Publications
2026
ERBB2 activating mutations and co-occurring genomic alterations contribute to disease heterogeneity in patients with ERBB2-mutant lung cancer.
Stockhammer P, El Zarif T, Schillo JL, Li F, Goldberg SB, Politi K, Grant MJ. ERBB2 activating mutations and co-occurring genomic alterations contribute to disease heterogeneity in patients with ERBB2-mutant lung cancer. J Thorac Oncol 2026, 103708. PMID: 41932614, DOI: 10.1016/j.jtho.2026.103708.Peer-Reviewed Original Research
2025
First-line immunotherapy with or without chemotherapy versus BRAF plus MEK inhibitors in BRAF V600E-mutated metastatic non-small-cell lung cancer (FRONT-BRAF): a multicentre, retrospective cohort study
Di Federico A, Wang K, Chen M, Barsouk A, Pagliaro A, Chen L, Ogliari F, Stockhammer P, Thawani R, Raslan S, Gariazzo E, Fusco F, Hambelton G, Citarella F, Meyer D, Aldea M, De Giglio A, Alessi J, Pecci F, Gelsomino F, Corassa M, Vokes N, Wang X, de Biase D, Abu Rous F, Areesawangkit P, Elghawy O, Cortellini A, Metro G, Ferrara R, Awad M, Pabani A, Murray J, Cappuzzo F, Garassino M, Dagogo-Jack I, Riely G, Grant M, Herzberg B, Ardizzoni A, Planchard D, Johnson B, Langer C, Offin M, Negrao M, Ricciuti B. First-line immunotherapy with or without chemotherapy versus BRAF plus MEK inhibitors in BRAF V600E-mutated metastatic non-small-cell lung cancer (FRONT-BRAF): a multicentre, retrospective cohort study. The Lancet Oncology 2025, 26: 1357-1369. PMID: 41038185, DOI: 10.1016/s1470-2045(25)00409-7.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAntineoplastic Combined Chemotherapy ProtocolsCarcinoma, Non-Small-Cell LungFemaleHumansImmune Checkpoint InhibitorsImmunotherapyLung NeoplasmsMaleMiddle AgedMitogen-Activated Protein Kinase KinasesMutationProtein Kinase InhibitorsProto-Oncogene Proteins B-rafRetrospective StudiesConceptsNon-small-cell lung cancerImmune checkpoint inhibitorsFirst-line immune checkpoint inhibitorsMitogen-activated protein kinase inhibitorMedian overall survivalOverall survivalHistory of smokingRetrospective cohort studyMitogen-activated protein kinaseAssociated with longer median overall survivalMetastatic non-small-cell lung cancerLung cancerPD-L1 tumor proportion scoreCohort studyEastern Cooperative Oncology Group performance statusHigher PD-L1 expressionLonger median overall survivalFirst-line immunotherapyFrequency of adverse eventsTP53 co-mutationsTreated with BRAFPD-L1 expressionTumor proportion scoreSecond-line therapyFirst-line therapy
2024
Efficacy of Antibody Drug Conjugates Alone and in Combination with other Agents in Metastatic Urothelial Carcinoma: A Scoping Review
Grant M, Stockhammer P, Austin M, Nemeth Z, Petrylak D. Efficacy of Antibody Drug Conjugates Alone and in Combination with other Agents in Metastatic Urothelial Carcinoma: A Scoping Review. Bladder Cancer 2024, 10: 9-23. PMID: 38993528, PMCID: PMC11181835, DOI: 10.3233/blc-230070.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsMetastatic urothelial carcinomaAntibody-drug conjugatesClinical trialsUrothelial carcinomaCombination regimensDrug conjugatesSystematic reviewAnti-PD-1 agentsProspective therapeutic clinical trialsCochrane Central TrialsClinical trial cohortObjective response rateTherapeutic clinical trialsMeta-Analyses (PRISMA) statementNon-duplicated articlesPreferred Reporting ItemsComprehensive systematic reviewPotent cytotoxic payloadTrial cohortEnfortumab vedotinOvid EmbaseSacituzumab govitecanADC targetImpressive efficacyOvid MEDLINE
2023
Co-Occurring Alterations in Multiple Tumor Suppressor Genes Are Associated With Worse Outcomes in Patients With EGFR-Mutant Lung Cancer
Stockhammer P, Grant M, Wurtz A, Foggetti G, Expósito F, Gu J, Zhao H, Choi J, Chung S, Li F, Walther Z, Dietz J, Duffield E, Gettinger S, Politi K, Goldberg S. Co-Occurring Alterations in Multiple Tumor Suppressor Genes Are Associated With Worse Outcomes in Patients With EGFR-Mutant Lung Cancer. Journal Of Thoracic Oncology 2023, 19: 240-251. PMID: 37806385, PMCID: PMC11364167, DOI: 10.1016/j.jtho.2023.10.001.Peer-Reviewed Original ResearchProgression-free survivalEGFR-mutant NSCLCTP53 mutationsOverall survivalClinical outcomesEGFR-TKIInferior outcomesWorse outcomesYale cohortMetastatic EGFR-mutant NSCLCShorter progression-free survivalEGFR-mutant lung cancerTyrosine kinase inhibitor therapyFirst-line TKIYale Cancer CenterSecond-line therapyInferior clinical outcomesSubset of patientsKinase inhibitor therapyAdditional therapeutic interventionsAggressive disease phenotypeCo-occurring alterationsTumor suppressor gene alterationsTumor genomic profilingMultiple tumor suppressor genesKrebs 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 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
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
Academic Achievements & Community Involvement
News
News
- June 10, 2026
Four Trainees Given Young Investigator Awards
- June 02, 2026
Yale Cancer Center Researchers and Trainees Present at 2026 ASCO Annual Meeting
- August 14, 2024
Welcome New Staff, Faculty, Fellows, Postgrads & Postdocs (August 2024)
- August 10, 2023Source: OncLive
Dr. Paul Stockhammer on Gene Alterations and Poor Outcomes in EGFR-Mutant Lung Cancer