ABSTRACT
Anaplastic lymphoma kinase (ALK) was originally identified in 1994 as a tyrosine kinase activated by a chromosomal translocation in an uncommon T cell lymphoma called anaplastic large-cell lymphoma (ALCL) [1]. Following its subsequent identification in a subset of non-small cell lung cancers (NSCLCs) in 2007 [2,3], ALK has emerged as a readily identifiable and therapeutically tractable molecular target in cancer [4]. Activation of ALK, which occurs primarily through gene rearrangements and point mutations, is found in a spectrum of diseases including ALCL [1], NSCLC [2,3], inflammatory myofibroblastic tumors (IMTs) [5], and neuroblastoma [6]. A variety of approaches to target ALK are in development, the most advanced of which is the ALK tyrosine kinase inhibitor crizotinib.
