Katerina Politi, PhD
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Appointments
Pathology
Primary
Medical Oncology
Secondary
Titles
Co-Leader, Cancer Signaling Networks, Yale Cancer Center; Scientific Director, Center for Thoracic Cancers
Contact Info
Appointments
Pathology
Primary
Medical Oncology
Secondary
Titles
Co-Leader, Cancer Signaling Networks, Yale Cancer Center; Scientific Director, Center for Thoracic Cancers
Contact Info
Appointments
Pathology
Primary
Medical Oncology
Secondary
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 CancersBiography
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
ProfessorSecondary
Other Departments & Organizations
- Cancer Signaling Networks
- Internal Medicine
- K12 Calabresi Immuno-Oncology Training Program (IOTP)
- Medical Oncology
- Molecular Medicine, Pharmacology, and Physiology
- 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 Subject Headings (MeSH)
Cell Transformation, Neoplastic; Lung Neoplasms; Molecular Targeted Therapy; Pathology
ORCID
0000-0001-6064-4527
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
Robert Homer, MD, PhD
Michael Grant, MD
Don Nguyen, PhD, BSc
Scott Gettinger, MD
31Publications
310Citations
Lung Neoplasms
Cell Transformation, Neoplastic
Molecular Targeted Therapy
Publications
2024
Overexpression 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, DOI: 10.1126/sciimmunol.adh5462.Peer-Reviewed Original ResearchAltmetricMeSH 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 deruxtecanThe Evolution of Mouse Models of Cancer: Past, Present, and Future.
Abate-Shen C, Politi K. The Evolution of Mouse Models of Cancer: Past, Present, and Future. Cold Spring Harbor Perspectives In Medicine 2024, a041736. PMID: 38772706, DOI: 10.1101/cshperspect.a041736.Peer-Reviewed Original ResearchAltmetricPlasticity-induced repression of Irf6 underlies acquired resistance to cancer immunotherapy in pancreatic ductal adenocarcinoma
Kim I, Diamond M, Yuan S, Kemp S, Kahn B, Li Q, Lin J, Li J, Norgard R, Thomas S, Merolle M, Katsuda T, Tobias J, Baslan T, Politi K, Vonderheide R, Stanger B. Plasticity-induced repression of Irf6 underlies acquired resistance to cancer immunotherapy in pancreatic ductal adenocarcinoma. Nature Communications 2024, 15: 1532. PMID: 38378697, PMCID: PMC10879147, DOI: 10.1038/s41467-024-46048-7.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsPancreatic ductal adenocarcinomaEpithelial-to-mesenchymal transitionResistance to immunotherapyT cell killingDuctal adenocarcinomaAcquired resistance to immunotherapyResistance to cancer immunotherapyMouse model of pancreatic ductal adenocarcinomaModel of pancreatic ductal adenocarcinomaExpression of immune checkpointsInterferon regulatory factor 6Effect of TNF-aEMT transcription factor ZEB1Antigen presentation machineryTumor immune microenvironmentCell-intrinsic defectsPro-apoptotic effectsPresentation machineryCancer immunotherapyImmune checkpointsTumor relapseImmune microenvironmentPrimary resistanceT cellsAcquired resistanceASCL1 Drives Tolerance to Osimertinib in EGFR Mutant Lung Cancer in Permissive Cellular Contexts.
Hu B, Wiesehöfer M, de Miguel F, Liu Z, Chan L, Choi J, Melnick M, Arnal Estape A, Walther Z, Zhao D, Lopez-Giraldez F, Wurtz A, Cai G, Fan R, Gettinger S, Xiao A, Yan Q, Homer R, Nguyen D, Politi K. ASCL1 Drives Tolerance to Osimertinib in EGFR Mutant Lung Cancer in Permissive Cellular Contexts. Cancer Research 2024, 84: 1303-1319. PMID: 38359163, PMCID: PMC11142404, DOI: 10.1158/0008-5472.can-23-0438.Peer-Reviewed Original ResearchCitationsAltmetricConceptsTyrosine kinase inhibitorsPatient-derived xenograftsEGFR mutant lung cancerMutant lung cancerPre-treatment tumorsResidual diseaseDrug toleranceLung cancerResidual tumor cells in vivoEGFR mutant lung adenocarcinomaTyrosine kinase inhibitor osimertinibEGFR tyrosine kinase inhibitorsTyrosine kinase inhibitor treatmentTumor cells in vivoMutant lung adenocarcinomaMaximal tumor regressionTranscription factor Ascl1Drug-tolerant cellsTime of maximal responseEvidence of cellsCells in vivoOsimertinib treatmentTumor regressionSingle cell transcriptional profilingTumor cellsPatient-Derived Models of Cancer in the NCI PDMC Consortium: Selection, Pitfalls, and Practical Recommendations
Habowski A, Budagavi D, Scherer S, Aurora A, Caligiuri G, Flynn W, Langer E, Brody J, Sears R, Foggetti G, Estape A, Nguyen D, Politi K, Shen X, Hsu D, Peehl D, Kurhanewicz J, Sriram R, Suarez M, Xiao S, Du Y, Li X, Navone N, Labanca E, Willey C. Patient-Derived Models of Cancer in the NCI PDMC Consortium: Selection, Pitfalls, and Practical Recommendations. Cancers 2024, 16: 565. PMID: 38339316, PMCID: PMC10854945, DOI: 10.3390/cancers16030565.Peer-Reviewed Original ResearchCitationsAltmetricConceptsPatient-derived models of cancerPatient-derived modelsModels of cancerThe National Institutes of HealthCancer modelsNational Cancer Institute of the National Institutes of HealthPrecision medicine programsNational Institutes of HealthNational Cancer InstituteInstitutes of HealthPreclinical cancer modelsMedicine programsDivision of Cancer BiologyIn vitroIn vivo model systemsPractice recommendationsDevelopment of novel model systemsClinical practiceStudies of human pathologyNovel model systemsSeries of vignettesModel systemCancer therapeuticsCancer biologyCancerEGFR-driven lung adenocarcinomas coopt alveolar macrophage metabolism and function to support EGFR signaling and growth.
Kuhlmann-Hogan A, Cordes T, Xu Z, Kuna R, Traina K, Robles-Oteiza C, Ayeni D, Kwong E, Levy S, Globig A, Nobari M, Cheng G, Leibel S, Homer R, Shaw R, Metallo C, Politi K, Kaech S. EGFR-driven lung adenocarcinomas coopt alveolar macrophage metabolism and function to support EGFR signaling and growth. Cancer Discovery 2024, 14: 524-545. PMID: 38241033, DOI: 10.1158/2159-8290.cd-23-0434.Peer-Reviewed Original ResearchCitationsConceptsLung adenocarcinomaGM-CSFEGFR-mutant lung adenocarcinomaGM-CSF secretionProinflammatory immune responseSuppress tumor progressionLocal immunosuppressionStatin therapyTherapeutic combinationsNovel therapiesTumor cellsTumor progressionTumor growthLung adenocarcinoma cellsEGFR phosphorylationImmune responseTransformed epitheliumCancer cellsInflammatory functionsEGFR signalingMacrophage metabolismAlveolar macrophagesIncreased cholesterol synthesisMetabolic supportOncogenic signalingEGFR-Driven Lung Adenocarcinomas Co-opt Alveolar Macrophage Metabolism and Function to Support EGFR Signaling and Growth.
Kuhlmann-Hogan A, Cordes T, Xu Z, Kuna R, Traina K, Robles-Oteíza C, Ayeni D, Kwong E, Levy S, Globig A, Nobari M, Cheng G, Leibel S, Homer R, Shaw R, Metallo C, Politi K, Kaech S. EGFR-Driven Lung Adenocarcinomas Co-opt Alveolar Macrophage Metabolism and Function to Support EGFR Signaling and Growth. Cancer Discovery 2024, of1-of22. PMID: 38270272, DOI: 10.1158/2159-8290.cd-23-0434.Peer-Reviewed Original ResearchCitationsAltmetricConceptsLung adenocarcinomaGM-CSFEGFR-mutant lung adenocarcinomaT cell-based immunotherapyTransformed epitheliumOncogenic signalingGM-CSF secretionProinflammatory immune responseSuppress tumor progressionLocal immunosuppressionStatin therapyTherapeutic combinationsNovel therapiesTumor cellsTumor progressionTumor growthLung cancerLung adenocarcinoma cellsEGFR phosphorylationImmune responseImmunological supportCancer cellsInflammatory functionsAlveolar macrophagesIncreased cholesterol synthesis
2023
Oncogenic context shapes the fitness landscape of tumor suppression
Blair L, Juan J, Sebastian L, Tran V, Nie W, Wall G, Gerceker M, Lai I, Apilado E, Grenot G, Amar D, Foggetti G, Do Carmo M, Ugur Z, Deng D, Chenchik A, Paz Zafra M, Dow L, Politi K, MacQuitty J, Petrov D, Winslow M, Rosen M, Winters I. Oncogenic context shapes the fitness landscape of tumor suppression. Nature Communications 2023, 14: 6422. PMID: 37828026, PMCID: PMC10570323, DOI: 10.1038/s41467-023-42156-y.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsCo-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, DOI: 10.1016/j.jtho.2023.10.001.Peer-Reviewed Original ResearchCitationsAltmetricConceptsProgression-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 genes
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
Links & Media
News
- July 16, 2024
YCC 2024 Trainee Colloquium
- July 08, 2024Source: The Cancer Letter
The early days of EGFR: Herbst, Haber, Meyerson, Pao, Sequist present at Yale SPORE workshop
- July 05, 2024Source: The Cancer Letter
At Lung SPORE Workshop, experts reflect on the significance of discovery of EGFR mutations two decades ago
- June 21, 2024
Yale Hosts Annual Lung Cancer SPORE Workshop
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