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. 2022 Apr 22;16(10):2000–2014. doi: 10.1002/1878-0261.13214

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© 2022 Genentech, Inc. Molecular Oncology published by John Wiley & Sons Ltd on behalf of Federation of European Biochemical Societies.

This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

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Fig. 4 — Mechanisms of acquired resistance to TKIs in NTRK‐fp solid tumours and ROS1‐fp NSCLC: (A) On‐target resistance; (B) Off‐target resistance. Black square indicates clinical resistance observed following treatment with therapeutic. ^aDual mutation. ^bFunctional domain/structure not reported/unknown. ^cSpecific mutation unknown/not reported. ^dReported in patients with ALK fusion‐positive lung cancer only. ^eComplete genomic profile of transformed SCLC not fully elucidated. ALK, anaplastic lymphoma kinase; BDNF, brain‐derived neurotrophic factor; C, crizotinib; DFG, Asp‐Phe‐Gly motif; E, entrectinib; KIT, KIT proto‐oncogene, receptor tyrosine kinase; KRAS, Kirsten rat sarcoma virus; L, larotrectinib; MET, mesenchymal epithelial transition; NGF, nerve growth factor beta; NRAS, neuroblastoma RAS viral (v‐ras) oncogene homolog; NTF‐3, Neurotrophin‐3; TKI, tyrosine kinase inhibitor; Trk, tropomyosin receptor kinase.