Aberrant ALK activity arises through fusions, point mutations, overexpression or amplifications and has been shown to be an oncogenic driver in a number of cancers including anaplastic large cell lymphoma (ALCL), non-small cell lung cancer (NSCLC), inflammatory myofibroblastic tumors (IMTs) neuroblastomas and more (reviewed in Della Corte et al, 2018; Lin et al, 2017). As a result, ALK is a promising therapeutic target for inhibition with tyrosine kinase inhibitors. Crizotinib, ceritinib, brigatinib, alectinib and lorlatinib are all approved for the treatment of ALK-driven cancers, however resistance commonly develops either as a result of accumulating secondary mutations, or through activation of bypass pathways that remove the dependence on ALK signaling (reviewed in Della Corte et al, 2017; Roskoski, 2013; Lin et al, 2017).
Troiani, T, Viscardi, G, Morgillo, F, Fasano, M, Martinelli, E, Ciardiello, F, Della Corte, CM, Di Liello, R
Roskoski, R
Shaw, AT, Riely, GJ, Lin, JJ
© 2022 Reactome
