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Nat. Rev. Clin. Oncol. doi:10.1038/nrclinonc.2017.127 Figure 2 Structural modelling of putative targeted therapy resistance mutations Figure 2 | Structural modelling of putative targeted therapy resistance mutations. a | In silico structural modelling of the tyrosine-kinase domains of ALK, ROS1, RET, TRKA, TRKB, and TRKC indicates a wide range of resistance mutations that cluster within regions including the ATP-binding pocket and the solvent front. The amino acids that replace wild-type residues following mutation are shown in red. b | Homology alignment demonstrates that several of the identified resistance mutations arise in paralogous residues across genes, suggesting that similar mechanisms of drug resistance can develop across different fusions. c | Most resistance mutations seen in ROS1, RET, TRKA, TRKB, and TRKC have paralogous resistance mutations identified in ALK. The specific paralogous amino acids shown in part b are listed here. Schram, A. M. et al. (2017) Fusions in solid tumours: diagnostic strategies, targeted therapy, and acquired resistance Nat. Rev. Clin. Oncol. doi:10.1038/nrclinonc.2017.127