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26-07-2017 | Non-small cell lung cancer | Editorial | Article

Changing landscape of treatment for ALK-positive non-small cell lung cancer

Fiona Blackhall
It is only 10 years since rearrangements in the anaplastic lymphoma kinase (ALK) gene were identified as the oncogenic driver in 3–7% of patients with non-small cell lung cancer (NSCLC) [1]. The majority of patients with ALK-rearranged NSCLC have adenocarcinoma histology, a history of never or light smoking, and are of relatively younger age [2]. Crizotinib, an oral small-molecule tyrosine kinase inhibitor (TKI) of ALK, MET and ROS1 kinases, was the first ALK inhibitor to enter clinical development [3]. On the basis of rapid and durable responses observed in early phase evaluation, crizotinib received accelerated approval from the United States Food and Drug Administration in 2011 [3–5]. The time interval between the discovery of ALK-rearranged NSCLC and approval of crizotinib was unprecedented and marked a new, long-awaited paradigm for oncology drug development.

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