Abstract IA18: Evolution of acquired resistance in EGFR mutant NSCLC

Lung cancers harboring activating EGFR mutations are exquisitely sensitive to EGFR tyrosine kinase inhibitors; however, acquired drug resistance inevitably develops. Although genetic mechanisms of acquired resistance have been well characterized, less is known about how resistant clones evolve during treatment. Emerging data are beginning to illuminate the complex interplay of genetic clonal heterogeneity, adaptive signaling changes, epigenetic plasticity, and microenvironment factors that shapes the evolution of acquired resistance. Novel therapeutic strategies that specifically target these processes may prevent or delay the development of drug resistance. Citation Format: Aaron N. Hata. Evolution of acquired resistance in EGFR mutant NSCLC [abstract]. In: Proceedings of the Fifth AACR-IASLC International Joint Conference: Lung Cancer Translational Science from the Bench to the Clinic; Jan 8-11, 2018; San Diego, CA. Philadelphia (PA): AACR; Clin Cancer Res 2018;24(17_Suppl):Abstract nr IA18.