Katerina Politi, PhD
Joseph A. and Lucille K. Madri Professor of PathologyCards
Appointments
Additional Titles
Co-Leader, Cancer Signaling Networks, Yale Cancer Center
Scientific Director, Center for Thoracic Cancers
Contact Info
Appointments
Additional Titles
Co-Leader, Cancer Signaling Networks, Yale Cancer Center
Scientific Director, Center for Thoracic Cancers
Contact Info
Appointments
Additional Titles
Co-Leader, Cancer Signaling Networks, Yale Cancer Center
Scientific Director, Center for Thoracic Cancers
Contact Info
About
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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.
Appointments
Pathology
ProfessorPrimaryMedical Oncology and Hematology
ProfessorSecondary
Other Departments & Organizations
- Cancer Signaling Networks
- Internal Medicine
- K12 Calabresi Immuno-Oncology Training Program (IOTP)
- 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
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Overview
Medical Research Interests
ORCID
0000-0001-6064-4527- View Lab Website
Politi Lab
Research at a Glance
Yale Co-Authors
Publications Timeline
Research Interests
Sarah Goldberg, MD, MPH
Anna Wurtz
Michael Grant, MD
Scott Gettinger, MD
Robert Homer, MD, PhD
Roy S. Herbst, MD, PhD
Lung Neoplasms
Cell Transformation, Neoplastic
Molecular Targeted Therapy
Publications
2025
Tolerance and resistance to targeted therapy in non-small cell lung cancer: Emerging concepts and strategies
Sanchez-Cespedes M, Lockwood W, Suda K, Gardner E, Mitsudomi T, Politi K, Rolfo C, Sen T, Sos M, Tammela T, Wynes M, Tsao M, Berger A. Tolerance and resistance to targeted therapy in non-small cell lung cancer: Emerging concepts and strategies. JTO Clinical And Research Reports 2025, 100944. DOI: 10.1016/j.jtocrr.2025.100944.Peer-Reviewed Original ResearchConceptsNon-small cell lung cancerInternational Association for the Study of Lung CancerCell lung cancerTargeted therapyLung cancerNon-genetic mechanismsDiscovery of EGFR mutationsApplication of targeted therapiesDrug-tolerant persister cellsClinical applicationLung cancer patientsStudy of Lung CancerCancer treatment todayTolerant persister cellsMechanisms of resistanceEGFR mutationsTumor toleranceTumor plasticityAcquired ResistanceDrug toleranceSomatic aberrationsCancer patientsTherapeutic approachesTherapyMicroenvironmental influencesEpigenetic priming promotes tyrosine kinase inhibitor resistance and oncogene amplification
Starble R, Sun E, Gbyli R, Radda J, Lu J, Jensen T, Sun N, Khudaverdyan N, Zhao T, Hu B, Melnick M, Zhao S, Roper N, Wang G, Tackett A, Wang Y, Song J, Politi K, Wang S, Xiao A. Epigenetic priming promotes tyrosine kinase inhibitor resistance and oncogene amplification. Nature Structural & Molecular Biology 2025, 1-13. PMID: 41131337, DOI: 10.1038/s41594-025-01685-4.Peer-Reviewed Original ResearchCitationsAltmetricConceptsInter-TAD interactionsChromatin functionOncogene amplificationCopy numberChromatin regulatory functionsIncrease of H3K27acInner nuclear membraneLung adenocarcinomaExpression of tumor-promoting genesTKI resistanceCopy number gainGene copy numberAmplified lociChromatin signaturesCohesin depositionCohesin recruitmentCohesin loadingGenome stabilityTumor-promoting genesPhenotypic effectsMammalian cellsEndoplasmic reticulumDrug-naive cellsTyrosine kinase inhibitor resistanceTKI-resistant tumorsEP.08.46 Neoadjuvant Immunotherapy Improves Recurrence-Free Survival in Resectable Non-Small Cell Lung Cancer - a 10-Year Institutional Experience
Ermer T, Kim S, Goldberg S, Blasberg J, Boffa D, Herbst R, Politi K, Schalper K, Dacic S, Woodard G. EP.08.46 Neoadjuvant Immunotherapy Improves Recurrence-Free Survival in Resectable Non-Small Cell Lung Cancer - a 10-Year Institutional Experience. Journal Of Thoracic Oncology 2025, 20: s769. DOI: 10.1016/j.jtho.2025.09.1483.Peer-Reviewed Original ResearchLasering in on Uncommon EGFR Mutations
Kim S, Politi K, Goldberg S. Lasering in on Uncommon EGFR Mutations. Journal Of Thoracic Oncology 2025, 20: 1148-1151. PMID: 40914593, DOI: 10.1016/j.jtho.2025.06.014.Peer-Reviewed Original ResearchAltmetricThe Polycomb Protein EED Constrains the SCLC Neuroendocrine Phenotype and Drives Lung Cancer Histological Transformation
Li Y, Laimon Y, Cho H, Vivero M, De Oliveira G, Delcea A, Chen Y, Durmaz Y, Qiu X, Berchuck J, Bronson R, Li S, Ji H, Politi K, Freedman M, Long H, Signoretti S, Oser M. The Polycomb Protein EED Constrains the SCLC Neuroendocrine Phenotype and Drives Lung Cancer Histological Transformation. Journal Of Thoracic Oncology 2025, 20: s31-s32. DOI: 10.1016/j.jtho.2025.07.028.Peer-Reviewed Original ResearchIntratumoral 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 ResearchThis study investigates intratumoral IL12 mRNA therapy, showing it effectively reactivates immune responses in checkpoint inhibitor-resistant tumors, leading to significant complete responses, potentially benefiting cancer patients with resistant tumors.Redundancy 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 ResearchCitationsAltmetricMeSH 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 predictorsPP01.07 Alterations in Tumor Suppressor Genes are Associated With Aggressive Disease Phenotypes in EGFR-Mutant NSCLC
Stockhammer P, Sweeney K, Liu S, Halmos B, Uprety D, Elliott A, VanderWalde A, Politi K, Goldberg S, Grant M. PP01.07 Alterations in Tumor Suppressor Genes are Associated With Aggressive Disease Phenotypes in EGFR-Mutant NSCLC. Journal Of Thoracic Oncology 2025, 20: s5. DOI: 10.1016/j.jtho.2025.03.015.Peer-Reviewed Original ResearchQuantitative 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
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
News & Links
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Media
The Power of Progress in Lung Cancer
Dr. Roy Herbst shares the progress that has been made in lung cancer care and research at Smilow Cancer Hospital and Yale Cancer Center.
News
- November 18, 2025
Progress and Hope: Sharing the Latest Advances in Lung Cancer Care
- November 13, 2025
The Power of Progress in Lung Cancer
- September 18, 2025
Yale’s Lung Cancer SPORE Grant Renewed by National Cancer Institute
- May 26, 2025
National Cancer Research Month with Dr. Katerina Politi
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Contacts
Locations
Nathan Smith Building
Lab
315 Cedar Street
New Haven, CT 06510
Winchester Building
Academic Office
25 York Street, Rm 208
New Haven, CT 06511