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Despite improvements in cancer therapies in the past 50 years, neuroblastoma remainsa devastating clinical problem and a leading cause of childhood cancer deaths.Advances in treatments for children with high-risk neuroblastoma have, untilrecently, involved addition of cytotoxic therapy to dose-intensive regimens. In thisera of targeted therapies, substantial efforts have been made to identify optimaltargets for different types of cancer. The discovery of hereditary and somaticactivating mutations in the oncogene ALK has now placed neuroblastoma amongother cancers, such as melanoma and non-small-cell lung cancer (NSCLC), whichbenefit from therapies with oncogene-specific small-molecule tyrosine kinaseinhibitors. Crizotinib, a small-molecule inhibitor of ALK, has transformed thelandscape for the treatment of NSCLC harbouring ALK translocations and hasdemonstrated activity in preclinical models of ALK-driven neuroblastomas. However,inhibition of mutated ALK is complex when compared with translocated ALK andremains a therapeutic challenge. This Review discusses the biology of ALK in thedevelopment of neuroblastoma, preclinical and clinical progress with the use of ALKinhibitors and immunotherapy, challenges associated with resistance to suchtherapies and the steps being taken to overcome some of these hurdles.

Targeting ALK in neuroblastoma—preclinical and clinical advancements