Background: Originally discovered in lymphomas,1 the ALK fusion oncogene with gain-of-function cytoplasmic tyrosine kinase activity has since been identified as an oncogenic driver in 3% to 10% of patients with non–small cell lung cancer (NSCLC).2,3 FDA approval of crizotinib, a small molecule ALK tyrosine kinase inhibitor (TKI), only 3 years after the discovery of the ALK fusion oncogene represents one of the most rapid bench-to-bedside translational advances in the history of targeted cancer therapy.4 Among the many fusion partners that have been reported, EML4 is the most common gene partner of ALK through a paracentric inversion of chromosome 2 inv(2) (p21;p23). We previously reported that in a cohort of 200 NSCLC specimens, the EML4-ALK–positive transcripts included 109 variant 1 (V1; 54.5%), 20 V2 (10.0%), 68 V3 (34.0%), and 3 V5a (1.5%) variants.5 Most (n=188; 94.0%) EML4-ALK–positive NSCLC tumors had adenocarcinoma histology... Conclusions: To our knowledge, this is the first..... READ ARTICLE
Journal of National Comprehensive Cancer Network DOI:10.6004/jnccn.2019.7291
Authors: Jay Gong, Jeffrey P. Gregg, Weijie Ma, Ken Yoneda, Elizabeth H. Moore, Megan E. Daly, Yanhong Zhang, Melissa J. Williams, Tianhong Li