Abstract
Rearrangements of the anaplastic lymphoma kinase (ALK) gene, which encodes for the ALK receptor tyrosine kinase, are detected in ∼5% of patients with non-small-cell lung cancer (NSCLC) with adenocarcinoma histology.1 Crizotinib was the first ALK tyrosine kinase inhibitor (TKI) approved for metastatic, ALK-positive NSCLC and was superior to platinum-based therapy in the first-line setting. However, crizotinib resistance develops due to secondary mutations in the ALK tyrosine kinase domain, ALK amplification, or activation of bypass pathways.
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