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thoracic-oncology / thoracic-oncologyEGFR Resistance Mechanisms

Katerina Politi

卡特琳娜·波利蒂

PhD

🏢Yale School of Medicine / Yale Cancer Center(耶鲁大学医学院 / 耶鲁癌症中心)🌐USA

Professor of Pathology and Medicine; Co-Director, Center for Thoracic Cancers病理学与医学教授;胸部肿瘤中心联合主任

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h-index
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Key Papers
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Awards
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Key Contributions

👥Biography 个人简介

Dr. Katerina Politi is a leading cancer biologist who developed foundational mouse models of EGFR-mutant lung cancer and has systematically dissected mechanisms of osimertinib resistance. Her translational research accelerates the development of next-generation lung cancer therapies.

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🧪Research Fields 研究领域

Thoracic Oncology胸部肿瘤学
EGFR ResistanceEGFR耐药机制
Osimertinib奥希替尼
Tumor Evolution肿瘤演化
Preclinical Models临床前模型

🎓Key Contributions 主要贡献

Genetically Engineered Mouse Models of EGFR-Mutant Lung Cancer

Created highly predictive mouse models of EGFR-driven NSCLC that recapitulate human disease and drug responses, enabling mechanistic study of targeted therapy and resistance in vivo.

Osimertinib Resistance Mechanisms

Identified EGFR amplification, MET amplification, and epithelial-mesenchymal transition as key osimertinib resistance mechanisms, providing rationale for combination approaches to delay or overcome resistance.

Tumor Heterogeneity and Clonal Evolution

Characterized clonal dynamics and intra-tumor heterogeneity in EGFR-mutant NSCLC under therapeutic pressure, informing concepts of adaptive therapy and minimal residual disease monitoring.

Representative Works 代表性著作

[1]

Lung Adenocarcinomas Induced in Mice by Mutant EGF Receptors Previously Found in Human Lung Cancers

Cancer Cell (2006)

Foundational study establishing the first EGFR-mutant lung cancer mouse models, creating essential tools for the entire field of EGFR-targeted therapy research.

[2]

Mechanisms of Acquired Resistance to the EGFR Inhibitor Osimertinib

Cancer Discovery (2018)

Comprehensive genomic and functional dissection of osimertinib resistance, identifying actionable mechanisms including EGFR amplification and bypass signaling.

[3]

Co-occurring Genomic Alterations Define Major Subsets of KRAS-Mutant Lung Adenocarcinoma with Distinct Vulnerabilities

Cancer Cell (2019)

Revealed that co-mutations with KRAS define functionally distinct NSCLC subtypes with different therapeutic dependencies, guiding combination therapy strategies.

🏆Awards & Recognition 奖项与荣誉

🏆National Cancer Institute Outstanding Investigator Award
🏆Yale Cancer Center Research Award
🏆Lung Cancer Research Foundation Scientific Grant Award
🏆AACR-Johnson & Johnson Lung Cancer Innovation Science Award

📄Data Sources 数据来源

Last updated: 2026-01-15 | All information from publicly available academic sources

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