Understanding the Molecular and Cellular Mechanisms that Underlie the Conversion of EGFR Mutant Lung Adenocarcinomas to Small Cell Lung Cancer Upon Treatment with Tyrosine Kinase Inhibitors
Mary Ann C. Melnick, MS and Katerina Politi, Ph.D.
Department of Pathology and Yale Cancer Center, Yale School of Medicine, New Haven, CT, USA
BACKGROUND
- Somatic mutations in the Epidermal Growth Factor Receptor (EGFR) are seen in approximately 15% of lung adenocarcinomas
- Mutant EGFR lung cancers are sensitive to tyrosine kinase inhibitor (TKI) treatment
- Resistance emerges on average 10-14 months after initiation of TKI treatment
- Phenotypic switch from lung adenocar-cinoma to Small Cell Lung Cancer
(SCLC) is seen in 6% of acquired resist-ance cases1 - EGFR mutant SCLC is sensitive to chemotherapies used to treat SCLC
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