title: New targets in advanced NSCLC: EML4-ALK.
abstract: 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.
authors.affiliation: Massachusetts General Hospital Cancer Center Center, Boston, MA 02114, USA.
authors.forename: Adam S
authors.initials: AS
authors.lastname: Crystal
authors.forename: Alice T
authors.initials: AT
authors.lastname: Shaw
mesh_terms: D002289:Carcinoma, Non-Small-Cell Lung / Q000175:diagnosis / Q000453:epidemiology / Q000235:genetics / Q000378:metabolism / Q000628:therapy; D000077547:Crizotinib; D015316:Genetic Therapy; D006801:Humans; D008175:Lung Neoplasms / Q000175:diagnosis / Q000453:epidemiology / Q000235:genetics / Q000378:metabolism / Q000628:therapy; D015514:Oncogene Proteins, Fusion / Q000235:genetics* / Q000378:metabolism; D011720:Pyrazoles / Q000627:therapeutic use; D011725:Pyridines / Q000627:therapeutic use
chemical_list: C522504:EML4-ALK fusion protein, human; D015514:Oncogene Proteins, Fusion; D011720:Pyrazoles; D011725:Pyridines; D000077547:Crizotinib