• Yutao Liu, Tianfeng Liu, Nan Li, Tao Wang, Yue Pu, and Rui Lin.
• Department of Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
• Lung Cancer. 2019 Mar 1; 129: 92-94.

ObjectivesNon-small-cell lung cancer (NSCLC) has various driver mechanisms, including ROS1 rearrangement with different fusion patterns. There is a need to identify and evaluate new ROS1 fusions and the response to targeted therapy.Materials And MethodsA targeted next-generation sequencing (NGS) panel was used to analyze DNA extracted from tumor tissue and blood samples from an NSCLC patient. Results were validated using Sanger sequencing.ResultsWe found a novel ROS1 rearrangement form, namely a WNK1-ROS1 fusion. The transmembrane and kinase domains of ROS1 remained intact in this fusion. No EGFR, MET, KRAS, ALK, ROS1 or other NSCLC driver mutations were detected in the patient. The patient achieved a partial response after treatment with crizotinib. When disease progressed, ROS1 G2032R mutation-a classical mechanism of crizotinib resistance-was detected in the DNA sample extracted from the patient's plasma sample.ConclusionWe identified a novel WNK1-ROS1 fusion that was sensitive to crizotinib and developed an ROS1 G2032R mutation when the disease progressed. The WNK1-ROS1 rearrangement appeared to be a novel driver of the lung cancer.Copyright © 2018 Elsevier B.V. All rights reserved.

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