Katerina Politi, PhD
Joseph A. and Lucille K. Madri Professor of PathologyDownloadHi-Res Photo
Cards
Appointments
Pathology
Primary
Medical Oncology and Hematology
Secondary
Additional Titles
Co-Leader, Cancer Signaling Networks, Yale Cancer Center
Scientific Director, Center for Thoracic Cancers
Contact Info
Appointments
Pathology
Primary
Medical Oncology and Hematology
Secondary
Additional Titles
Co-Leader, Cancer Signaling Networks, Yale Cancer Center
Scientific Director, Center for Thoracic Cancers
Contact Info
Appointments
Pathology
Primary
Medical Oncology and Hematology
Secondary
Additional Titles
Co-Leader, Cancer Signaling Networks, Yale Cancer Center
Scientific Director, Center for Thoracic Cancers
Contact Info
About
Titles
Joseph A. and Lucille K. Madri Professor of Pathology
Co-Leader, Cancer Signaling Networks, Yale Cancer Center; Scientific Director, Center for Thoracic Cancers
Biography
Katerina Politi studied Biology at the University of Pavia in Italy. She then moved to New York, where she obtained her PhD in Genetics and Development working with Argiris Efstratiadis at Columbia University. Following graduate school, she joined Harold Varmus's lab at Memorial Sloan-Kettering Cancer Center and began her work on the molecular basis of lung cancer. She continues this work at Yale as a Professor in the Department of Pathology and Yale Cancer Center.
Last Updated on March 04, 2024.
Appointments
Pathology
ProfessorPrimaryMedical Oncology and Hematology
ProfessorSecondary
Other Departments & Organizations
- Cancer Signaling Networks
- Internal Medicine
- K12 Calabresi Immuno-Oncology Training Program (IOTP)
- Medical Oncology
- Medical Oncology and Hematology
- Molecular Medicine, Pharmacology, and Physiology
- MR Core
- Pathology
- Pathology and Molecular Medicine
- Pathology Research
- Politi Lab
- Program in Translational Biomedicine (PTB)
- SPORE in Lung Cancer
- Yale Cancer Center
- Yale Center for Immuno-Oncology
- Yale Combined Program in the Biological and Biomedical Sciences (BBS)
- Yale Stem Cell Center
- Yale Ventures
Education & Training
- Senior Research Scientist
- Memorial Sloan-Kettering Cancer Center (2010)
- Research Fellow
- Memorial Sloan-Kettering Cancer Center (2008)
- PhD
- Columbia University (2003)
- Postdoctoral Research Scientist
- Columbia University (2003)
Research
Overview
Medical Research Interests
Cell Transformation, Neoplastic; Lung Neoplasms; Molecular Targeted Therapy; Pathology
ORCID
0000-0001-6064-4527- View Lab Website
Politi Lab
Research at a Glance
Yale Co-Authors
Frequent collaborators of Katerina Politi's published research.
Publications Timeline
A big-picture view of Katerina Politi's research output by year.
Research Interests
Research topics Katerina Politi is interested in exploring.
Sarah Goldberg, MD, MPH
Anna Wurtz
Scott Gettinger, MD
Michael Grant, MD
Robert Homer, MD, PhD
Roy S. Herbst, MD, PhD
42Publications
669Citations
Lung Neoplasms
Cell Transformation, Neoplastic
Molecular Targeted Therapy
Publications
2025
Intratumoral IL12 mRNA administration activates innate and adaptive pathways in checkpoint inhibitor-resistant tumors resulting in complete responses
Lakshmipathi J, Santha S, Li M, Qian Y, Roy S, Luheshi N, Politi K, Bosenberg M, Eyles J, Muthusamy V. Intratumoral IL12 mRNA administration activates innate and adaptive pathways in checkpoint inhibitor-resistant tumors resulting in complete responses. Cancer Immunology, Immunotherapy 2025, 74: 250. PMID: 40560386, PMCID: PMC12198101, DOI: 10.1007/s00262-025-04105-0.Peer-Reviewed Original ResearchMeSH Keywords and ConceptsConceptsAnti-tumor immune responseTumor-associated macrophagesCytotoxic T cellsImmune responseActivity of checkpoint inhibitorsAnti-PD-L1 antibodyPhagocytosis of tumor cellsAnti-PD-L1Enhanced anti-tumorAntigen presentation machineryCell-based immune responsesMurine tumor modelsTh1-type cytokinesColorectal carcinoma tumorsICI resistanceMurine IL12Checkpoint inhibitorsPresentation machineryIntratumoral deliveryResistant tumorsAdvanced diseaseCarcinoma tumorsTumor microenvironmentMurine tumorsT cellsRedundancy of the OST catalytic subunit facilitates therapeutic targeting of N-glycosylation
Baro M, Lee H, Kelley V, Lou R, Phoomak C, Politi K, Zeiss C, Van Zandt M, Contessa J. Redundancy of the OST catalytic subunit facilitates therapeutic targeting of N-glycosylation. Cell Chemical Biology 2025, 32: 839-853.e6. PMID: 40494352, DOI: 10.1016/j.chembiol.2025.05.005.Peer-Reviewed Original ResearchAltmetricMeSH Keywords and ConceptsConceptsN-glycosylationTrafficking of cell surface receptorsInhibits N-glycosylationCell surface receptorsGlycan synthesisCatalytic subunitOligosaccharyltransferaseEnzymatic activitySurface receptorsSTT3BSTT3ACharacterized in vitroDownstream effectsLung cancer xenograftsTherapeutic targetPatient-derivedBiological activityTumor regressionCancer xenograftsSmall moleculesGrowth delayTherapeutic agentsGlycansClinical features associated with an exceptional response to immunotherapy in patients with metastatic non-small cell lung cancer (NSCLC).
Nie Y, Wurtz A, Li F, Schalper K, Duffield E, Rowen E, Gerrish H, Chiang A, Goldberg S, Wilson F, Kim S, Grant M, Sabbath K, Talsania A, Lasala J, Russo A, Politi K, Herbst R, Gettinger S. Clinical features associated with an exceptional response to immunotherapy in patients with metastatic non-small cell lung cancer (NSCLC). Journal Of Clinical Oncology 2025, 43: 8544-8544. DOI: 10.1200/jco.2025.43.16_suppl.8544.Peer-Reviewed Original ResearchConceptsMetastatic non-small cell lung cancerNon-small cell lung cancerMonocyte-to-lymphocyte ratioAbsolute lymphocyte countPre-treatment absolute lymphocyte countResponse to immunotherapyCell lung cancerExceptional respondersLiver metastasesImmunotherapy responseAdvanced non-small cell lung cancerLung cancerTumor PD-L1 expressionPresence of brain metastasesInfluence immunotherapy responsivenessPD-L1 expressionSubsets of patientsTumor microenvironment analysisYale Cancer CenterTumor tissue analysisIRB-approved protocolLong-term survivalConcurrent chemotherapyBrain metastasesClinicopathological predictorsQuantitative Protein Expression of Antibody-Drug Conjugate Targets in EGFR Mutated and Wild-type Non-Small Cell Lung Cancer.
Trontzas I, He M, Wurtz A, Robbins C, Robinson N, Bates K, Liu M, Aung T, Scott L, Chan N, Burela S, Schillo J, Liebler D, Hill S, Morrison R, Vathiotis I, Syrigos K, Goldberg S, Politi K, Rimm D. Quantitative Protein Expression of Antibody-Drug Conjugate Targets in EGFR Mutated and Wild-type Non-Small Cell Lung Cancer. Clinical Cancer Research 2025, 31: 2767-2776. PMID: 40047548, PMCID: PMC12213210, DOI: 10.1158/1078-0432.ccr-24-3347.Peer-Reviewed Original ResearchCitationsAltmetricConceptsNon-small cell lung cancerAntibody-drug conjugatesAntibody-drug conjugate targetsEGFR mutationsCell lung cancerEGFR expressionQuantitative immunofluorescenceWild-type non-small cell lung cancerLung cancerAssociated with EGFR mutationsAssociated with EGFR expressionTissue microarray cohortAssociation of HER2Management of patientsAssay limitProportion of casesMutation statusTROP2 expressionMicroarray cohortEGFRQuantitative protein expressionTreatment sequencePatientsCell linesWild-type
2024
Hypoxia is linked to acquired resistance to immune checkpoint inhibitors in lung cancer
Robles-Oteíza C, Hastings K, Choi J, Sirois I, Ravi A, Expósito F, de Miguel F, Knight J, López-Giráldez F, Choi H, Socci N, Merghoub T, Awad M, Getz G, Gainor J, Hellmann M, Caron É, Kaech S, Politi K. Hypoxia is linked to acquired resistance to immune checkpoint inhibitors in lung cancer. Journal Of Experimental Medicine 2024, 222: e20231106. PMID: 39585348, PMCID: PMC11602551, DOI: 10.1084/jem.20231106.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsImmune checkpoint inhibitorsNon-small cell lung cancerAcquired resistanceCheckpoint inhibitorsResistant tumorsPatients treated with anti-PD-1/PD-L1 therapyAnti-PD-1/PD-L1 therapyLung cancerResistance to immune checkpoint inhibitorsAssociated with decreased progression-free survivalHypoxia activated pro-drugsTargeting hypoxic tumor regionsTreat non-small cell lung cancerAnti-CTLA-4Anti-PD-1Immune checkpoint inhibitionTumor metabolic featuresProgression-free survivalCell lung cancerResistant cancer cellsHypoxic tumor regionsMHC-II levelsRegions of hypoxiaKnock-outCheckpoint inhibitionEP.07C.10 Real-World Outcomes of Patients Treated with Neoadjuvant Immunotherapy for Resectable Non-Small Cell Lung Cancer
Ermer T, Kim S, Goldberg S, Zolfaghari E, Blasberg J, Boffa D, Herbst R, Politi K, Schalper K, Dacic S, Woodard G. EP.07C.10 Real-World Outcomes of Patients Treated with Neoadjuvant Immunotherapy for Resectable Non-Small Cell Lung Cancer. Journal Of Thoracic Oncology 2024, 19: s543-s544. DOI: 10.1016/j.jtho.2024.09.1007.Peer-Reviewed Original ResearchChitinase 3-like-1 (CHI3L1) in the pathogenesis of epidermal growth factor receptor mutant non-small cell lung cancer
Kamle S, Ma B, Schor G, Bailey M, Pham B, Cho I, Khan H, Azzoli C, Hofstetter M, Sadanaga T, Herbst R, Politi K, Lee C, Elias J. Chitinase 3-like-1 (CHI3L1) in the pathogenesis of epidermal growth factor receptor mutant non-small cell lung cancer. Translational Oncology 2024, 49: 102108. PMID: 39178575, PMCID: PMC11388375, DOI: 10.1016/j.tranon.2024.102108.Peer-Reviewed Original ResearchCitationsAltmetricConceptsNon-small cell lung cancerEpidermal growth factor receptorTyrosine kinase inhibitorsEpidermal growth factor receptor mutant non-small cell lung cancerMutant non-small cell lung cancerEpidermal growth factor receptor axisCell lung cancerLung cancerTherapeutic resistanceDownstream targets of EGFRResistance to TKI therapyEpithelial cellsStimulated epidermal growth factor receptorWild type epidermal growth factor receptorTargeting of epidermal growth factor receptorActivating EGFR mutationsChitinase 3-like 1Progression free survivalInduce tumor cell deathEpidermal growth factor receptor activationEffects of EGFR activationInhibited pulmonary metastasisTumor cell deathResponse to treatmentGrowth factor receptorAuthor Correction: Mechanisms and clinical activity of an EGFR and HER2 exon 20–selective kinase inhibitor in non–small cell lung cancer
Robichaux J, Elamin Y, Tan Z, Carter B, Zhang S, Liu S, Li S, Chen T, Poteete A, Estrada-Bernal A, Le A, Truini A, Nilsson M, Sun H, Roarty E, Goldberg S, Brahmer J, Altan M, Lu C, Papadimitrakopoulou V, Politi K, Doebele R, Wong K, Heymach J. Author Correction: Mechanisms and clinical activity of an EGFR and HER2 exon 20–selective kinase inhibitor in non–small cell lung cancer. Nature Medicine 2024, 30: 2694-2695. PMID: 39164519, DOI: 10.1038/s41591-024-03178-1.Peer-Reviewed Original ResearchAltmetricOverexpression 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, PMCID: PMC12087577, DOI: 10.1126/sciimmunol.adh5462.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsTumor 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 1MicroenvironmentComprehensive 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 ResearchConceptsNon-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 deruxtecan
Clinical Trials
Current Trials
Determining Mechanisms of Sensitivity and Resistance to Anti-Cancer Therapy for Advanced Lung Cancer
HIC ID1603017333RoleSub InvestigatorPrimary Completion Date06/20/2026Recruiting Participants
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315 Cedar Street
New Haven, CT 06510
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New Haven, CT 06511