MA02.04 Molecular Drivers and Therapeutic Targets for Neuroendocrine Transformation in Lung Cancer

Abstract

Histological transformation from lung adenocarcinoma (LUAD) to an aggressive neuroendocrine (NE) derivative resembling small cell carcinoma (SCLC) is a signature example of lineage plasticity in cancer. NE transformation is the primary mechanism of acquired resistance in up to 14% of EGFR-mutant LUADs. Despite this high prevalence, little is known about the molecular alterations occurring during NE transformation in human tumors. The high prevalence, together with the fact that transformed SCLC has a notably poor prognosis, make in-depth understanding of NE transformation in lung cancer highly clinically relevant and a critical need.