TPD52L1-ROS1 Rearrangement as a New Acquired Resistance Mechanism to Osimertinib That Responds to Crizotinib in Combination With Osimertinib in Lung Adenocarcinoma
Caihua Xu, Dapeng Li, Weiming Duan, Min Tao
Abstract
Osimertinib was approved for the treatment of patients with NSCLC with EGFR T790M mutation, revealing both progression-free and overall survival benefits in first- and second-line settings.1 However, resistance to osimertinib inevitably develops because of various mechanisms. One of the most common mechanisms is mutation at osimertinib’s primary target residue C797 that impedes binding of the drug to EGFR, particularly in a cis position. Subsequently, several studies have reported mutations at G796R/S, L792 (in trans with C797), and L718Q/V that compromise the efficacy of osimertinib.
Topics & Concepts
OsimertinibCrizotinibT790MLung cancerAdenocarcinomaMedicineCancer researchOncologyInternal medicineCancerROS1Malignant pleural effusionLung Cancer Treatments and MutationsColorectal Cancer Treatments and StudiesPI3K/AKT/mTOR signaling in cancer