The anaplastic lymphoma kinase (ALK) gene plays an important physiologic role in the development of the brain and can be oncogenically altered in several malignancies, including non-small-cell lung cancer (NSCLC) and anaplastic large cell lymphomas (ALCL). Most prevalent ALK alterations are chromosomal rearrangements resulting in fusion genes, as seen in ALCL and NSCLC. In other tumors, ALK copy-number gains and activating ALK mutations have been described. Dramatic and often prolonged responses are seen in patients with ALK alterations when treated with ALK inhibitors. Three of these—crizotinib, ceritinib, and alectinib—are now FDA approved for the treatment of metastatic NSCLC positive for ALK fusions. However, the emergence of resistance is universal. Newer ALK inhibitors and other targeting strategies are being developed to counteract the newly emergent mechanism(s) of ALK inhibitor resistance. This review outlines the recent developments in our understanding and treatment of tumors with ALK alterations.
ALK: a tyrosine kinase target for cancer therapy
V. Holla,Y. Elamin,Ann M. Bailey,Amber M. Johnson,B. Litzenburger,Yekaterina Khotskaya,Nora S. Sanchez,Jia Zeng,Md Abu Shufean,K. Shaw,J. Mendelsohn,G. Mills,F. Meric-Bernstam,G. Simon
Published 2017 in Cold Spring Harbor molecular case studies
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- Publication year
2017
- Venue
Cold Spring Harbor molecular case studies
- Publication date
2017-01-01
- Fields of study
Medicine
- Identifiers
- External record
- Source metadata
Semantic Scholar, PubMed
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