Combined blockade of GPX4 and activated EGFR/HER3 bypass pathways inhibits the development of ALK‐inhibitor‐induced tolerant persister cells in ALK‐fusion‐positive lung cancer

Cancers can develop resistance to treatment with ALK tyrosine kinase inhibitors (ALK-TKIs) via emergence of a subpopulation of drug-tolerant persister (DTP) cells that can survive initial drug treatment long enough to acquire genetic aberrations. DTP cells are thus a potential therapeutic target. We generated alectinib-induced DTP cells from a patient-derived ALK