Emergence of Preexisting MET Y1230C Mutation as a Resistance Mechanism to Crizotinib in NSCLC with MET Exon 14 Skipping Sai-Hong Ignatius Ou, MD, PhD, Lauren Young, MS, Alexa B. Schrock, PhD, Adrienne Johnson, BS, Samuel J. Klempner, MD, Viola W. Zhu, MD, PhD, Vincent A. Miller, MD, Siraj M. Ali, MD, PhD Journal of Thoracic Oncology Volume 12, Issue 1, Pages 137-140 (January 2017) DOI: 10.1016/j.jtho.2016.09.119 Copyright © 2016 International Association for the Study of Lung Cancer Terms and Conditions
Figure 1 Computed tomography scans of the patient before crizotinib treatment, confirmed response to crizotinib, and at progression during crizotinib treatment. Journal of Thoracic Oncology 2017 12, 137-140DOI: (10.1016/j.jtho.2016.09.119) Copyright © 2016 International Association for the Study of Lung Cancer Terms and Conditions
Figure 2 Comprehensive genomic profiling profiling of a pre–crizotinib treatment tumor tissue sample showing MNNG HOS Transforming gene (MET) exon 14 skipping alteration (D1010H) and the presence of Y1230C mutation (red circle) at a very low frequency (upper panel). Circulating tumor DNA assay detecting the presence of the original MET exon 14 skipping alteration and the Y1230C resistance mutation, both at reportable levels (lower panel). Percentages indicate the mutant allele frequency for the given assay. Journal of Thoracic Oncology 2017 12, 137-140DOI: (10.1016/j.jtho.2016.09.119) Copyright © 2016 International Association for the Study of Lung Cancer Terms and Conditions