Journal
CANCER LETTERS
Volume 351, Issue 2, Pages 215-221Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.canlet.2014.05.020
Keywords
NSCLC; ALK; ALK inhibitor; Drug resistance; Alectinib; Xenograft model
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The clinical efficacy of the ALK inhibitor crizotinib has been demonstrated in ALK fusion-positive NSCLC; however, resistance to crizotinib certainly occurs through ALK secondary mutations in clinical use. Here we examined the efficacy of a selective ALK inhibitor alectinib/CH5424802 in models of crizotinib resistance. Alectinib led to tumor size reduction in EML4-ALK-positive xenograft tumors that failed to regress fully during the treatment with crizotinib. In addition, alectinib inhibited the growth of some EML4-ALK mutant-driven tumors, including the G1269A model. These results demonstrated that alectinib might provide therapeutic opportunities for crizotinib-treated patients with ALK secondary mutations. (C) 2014 Elsevier Ireland Ltd. All rights reserved.
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