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
Deputy Director, Yale Cancer Center
Scientific Director, Center for Thoracic Cancers
Contact Info
Appointments
Pathology
Primary
Medical Oncology and Hematology
Secondary
Additional Titles
Deputy Director, Yale Cancer Center
Scientific Director, Center for Thoracic Cancers
Contact Info
Appointments
Pathology
Primary
Medical Oncology and Hematology
Secondary
Additional Titles
Deputy Director, 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
Deputy Director, 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 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
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
Francisco Exposito, PhD
Anna Wurtz
Don Nguyen, PhD
Michael Grant, MD
Robert Homer, MD, PhD
38Publications
1,089Citations
Lung Neoplasms
Cell Transformation, Neoplastic
Molecular Targeted Therapy
Publications
2026
Loss of PTEN as an Independent Poor Prognosis Indicator in Lung Adenocarcinoma, but Not in Squamous Cell Carcinoma, Is Associated with an Immunosuppressive Tumor Microenvironment and Distinct Co-Mutational Profiles
Houry M, Silva S, Artola M, Behrens C, Politi K, Wistuba I, Montuenga L, Exposito F, Calvo A. Loss of PTEN as an Independent Poor Prognosis Indicator in Lung Adenocarcinoma, but Not in Squamous Cell Carcinoma, Is Associated with an Immunosuppressive Tumor Microenvironment and Distinct Co-Mutational Profiles. Medical Sciences 2026, 14: 254. PMID: 42201046, PMCID: PMC13214857, DOI: 10.3390/medsci14020254.Peer-Reviewed Original ResearchMeSH Keywords and ConceptsConceptsNon-small cell lung cancerLung squamous cell carcinomaSquamous cell carcinomaLung adenocarcinomaOverall survivalTP53Prognostic significanceCell carcinomaCo-mutationsLung cancerConclusions:Associated with significantly worse overall survivalAssociated with shorter OSMethods:Significantly worse overall survivalNon-small cell lung cancer subtypesMultivariate Cox regression analysisAssociated with poor outcomesCo-mutation analysisSignificance of PTENImmunosuppressive tumor microenvironmentResected NSCLC patientsPoor prognosis indicatorT regulatory cellsCell lung cancerA Roadmap to Transform Lung Cancer Outcomes: Priorities in Biology, Therapeutic Innovation, Early Detection, Prevention and Interception
Winslow M, Ahmed M, Berg C, Black J, Downward J, Govindan R, Herbst R, Heymach J, Jaffee E, Kraut N, Merad M, Meyerson M, Pandya T, Politi K, Rao A, Rudin C, Soria J, Tang Y, Wong K, Yap T, Swanton C, Abbosh C, Bess B, Bivona T, Blackhall F, Brahmer J, Cheng I, Chuter D, De Koning H, Diehn M, Dive C, Galbraith S, Gros A, Jamal-Hanjani M, Janes S, Jänne P, Klebanoff C, Lee S, Lovly C, McGranahan N, Mok T, Peters S, Schalper K, Sequist L, Shaw A, Siu L, Solomon B, Spira A, Stiles B, Tan D, Temel J, Tsai C, Velculescu V, Vokes E, Whetstine J, Winn R, Chih-Hsin Yang J. A Roadmap to Transform Lung Cancer Outcomes: Priorities in Biology, Therapeutic Innovation, Early Detection, Prevention and Interception. Cancer Discovery 2026, 16: 1055-1073. PMID: 42001483, PMCID: PMC7619086, DOI: 10.1158/2159-8290.cd-25-2318.Peer-Reviewed Original ResearchAltmetricMeSH Keywords and ConceptsConceptsLung cancerGlobal cancer-related deathsDrug resistance mechanismsCancer-related deathsClinical trials databasesEarly detectionLung cancer subtypesLung cancer treatmentLung cancer outcomesLung cancer morbidityTask ForceEarly detection strategiesResearch prioritiesClinical trial designTargeted therapyPatient stratificationCancer subtypesTrials databasesCancer outcomesCancer morbidityNovel treatmentCancer treatmentPrevention initiativesLungUnmet needsERBB2 activating mutations and co-occurring genomic alterations contribute to disease heterogeneity in patients with ERBB2-mutant lung cancer
Stockhammer P, El Zarif T, Schillo J, Li F, Goldberg S, Politi K, Grant M. ERBB2 activating mutations and co-occurring genomic alterations contribute to disease heterogeneity in patients with ERBB2-mutant lung cancer. Journal Of Thoracic Oncology 2026, 103708. PMID: 41932614, DOI: 10.1016/j.jtho.2026.103708.Peer-Reviewed Original ResearchCitationsAltmetricConceptsFirst-line chemoimmunotherapyERBB2 mutationsTyrosine kinase domainNSCLC tumorsFH cohortCo-mutationsMedian tumor mutation burdenTyrosine kinase domain mutationsMultivariate Cox regression modelERBB2 activating mutationProgression-free survivalTumor mutational burdenExtracellular domainCharacteristics of patientsCox regression modelsFood and Drug AdministrationTrastuzumab deruxtecanMutational burdenMale patientsHigher RatesClinical outcomesSmoking historyActivating mutationsLung cancerGenomic alterations
2025
Tolerance and Resistance to Targeted Therapy in NSCLC: 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 NSCLC: Emerging Concepts and Strategies. JTO Clinical And Research Reports 2025, 7: 100944. PMID: 41858873, PMCID: PMC12996998, DOI: 10.1016/j.jtocrr.2025.100944.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsCitationsAltmetricConceptsNon-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, 33: 7-19. PMID: 41131337, PMCID: PMC12819156, 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 tumorsLasering 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.Commentaries, Editorials and LettersCitationsAltmetricIntratumoral 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, PMCID: PMC13107401, 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 agentsGlycansPreclinical Models of Solid Cancers for Testing Cancer Immunotherapies
Exposito F, Connolly K, Tang T, Chiorazzi M, Hunt B, Cardenas J, Nguyen D, Joshi N, Politi K. Preclinical Models of Solid Cancers for Testing Cancer Immunotherapies. Annual Review Of Cancer Biology 2025, 9: 285-305. DOI: 10.1146/annurev-cancerbio-062822-024810.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsCitationsConceptsResponse to immunotherapyDevelopment of immunotherapyStandard treatment optionCancer immunotherapy drugsCancer-immune interactionsNumerous cancer typesImmunotherapy resistanceImmunotherapy drugsCancer immunologyPreclinical modelsTreatment optionsMouse modelImmunotherapyCancer typesAdvanced in vitro systemsHuman modelTherapyCancerMiceImmunologyDrugQuantitative 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
IRB ID1603017333RoleSub InvestigatorPrimary Completion Date06/16/2036Recruiting 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
- June 16, 2026
Lung Cancer Scientific Symposium
- April 08, 2026
Lung Cancer: How Tumors Develop, Resist Treatment, and What Comes Next
- April 08, 2026
Center for Thoracic Cancers Hosts: Celebrate the Unexpected
- March 26, 2026Source: CASE
Connecticut Academy of Science and Engineering Elects 36 New Members in 2026
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Nathan Smith Building
Lab
315 Cedar Street
New Haven, CT 06510
Winchester Building
Academic Office
25 York Street, Rm 208
New Haven, CT 06511