Paradoxical functions of ZEB1 in EGFR-mutant lung cancer: tumor suppressor and driver of therapeutic resistance

Lung cancer is the leading cause of cancer-related death in the United States and worldwide. While the 5-year survival for lung cancer is a dismal 15%, there have been significant advances in treating patients with non-small cell lung cancer (NSCLC) in the past decade. These recent advances stem from the shift to classifying patients with NSCLC into distinct subtypes based upon the molecular driver, which include KRAS mutations (~25%), EGFR mutations (~15%), ALK translocations (~8%), and MET amplification/mutations (~6-7%) (1,2).