Abstract

Rearrangements in anaplastic lymphoma kinase ( ALK ) gene and echinoderm microtubule-associated protein-like 4 ( EML4 ) gene were first described in 2007. This genomic aberration is found in about 2–8% of non-small cell lung cancer (NSCLC) patients. In patients with adenocarcinoma lacking EGFR and KRAS mutations, the prevalence of EML4-ALK translocation could be as high as 42.8% (1). In these patients, ALK rearrangements serve as a key and strong oncogenic driver for NSCLC and represent a critical therapeutic target susceptible to targeted ALK kinase inhibition (2,3).

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