Targeted therapies aimed at inhibiting oncogenic tyrosine kinases are becoming commonplace in the treatment of cancer. The EML4-ALK fusion gene was first identified as a potentially targetable oncogenic driver in non-small cell lung cancer in 2007. A small molecule ALK inhibitor, crizotinib, may now be on the verge of approval by the US Food and Drug Administration for the treatment of ALK-rearranged lung cancer.
Here we review the discovery of EML4-ALK, the development of clinical diagnostics for ALK rearrangements, the clinical epidemiology of lung cancers driven by EML4-ALK, and ongoing ALK inhibitor-based clinical trials.
