Non-small cell lung cancer exhibits substantial histological and molecular heterogeneity. Alterations involving EGFR, ALK, ROS1, KRAS, BRAF, RET, MET, HER2, and other oncogenic drivers can continuously activate tumor-cell proliferation and survival signaling and generate molecular subtypes with ...
Tumor organoids can retain some of the histological features, driver alterations, and clonal differences of a patient’s tumor, providing expandable human-derived models for studying tumor evolution, therapeutic sensitivity, and mechanisms of drug resistance.