Chang-Min Choi

TL;DR: This first comprehensive study of somatic genome alterations in SCLC uncovers several key biological processes and identifies candidate therapeutic targets in this highly lethal form of cancer.

TL;DR: Increased activation of AXL and evidence for epithelial-to-mesenchymal transition (EMT) in multiple in vitro and in vivo EGFR-mutant lung cancer models with acquired resistance to erlotinib in the absence of the EGFR p.Thr790Met alteration or MET activation are reported.

TL;DR: It is shown that exosomes derived from lung cancer cells express PD-L1 and play a role in immune escape by reducing T-cell activity and promoting tumor growth, and indicates that tumor-derived exosome expressing PD- L1 may be an important mediator of tumor immune escape.

TL;DR: ALK rearrangement was not a significant prognostic factor in surgically resectable NSCLC and simultaneous tests for ALK IHC and EGFR mutation (Chung's SNUBH molecular test protocol), which has important implications for the storage and use of small biopsy or cytology samples for genetic analysis.

TL;DR: The efficacy of NPS-1034 is established in NSCLC cells rendered resistant to EGFR-TKIs because of MET or AXL activation or ROS1 rearrangement and in xenograft mouse models of HCC827/GR.