Abstract
The ALK fusion oncogene was first identified in non-small cell lung cancer (NSCLC) in 2007 (1). It has been identified in approximately 3–7% of NSCLC cases, and more commonly in younger patients, and non- or light smokers. The central nervous system (CNS) is the most common site of disease progression, with many incidences of brain metastases diagnosed at disease onset. In the last 10 years, the discovery of ALK rearrangements has led to the rapid emergence of various ALK inhibitors, many developed in response to ALK resistance mutations that develop to crizotinib and to improve responses in the CNS.
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