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. 2016 Apr 5;30(7):1493–1501. doi: 10.1038/leu.2016.51

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Copyright © 2016 Macmillan Publishers Limited

This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-nd/4.0/

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FOXO1 levels are elevated in a subset of relapsed patient samples and are sensitive to GDC-0941-mediated survival inhibition. (a) The baseline proteomic signature of TKI-naive samples (samples 180, 266 and 300) compared with samples from TKI-relapsed patients (resistant) lacking BCR–ABL1 mutations (samples 109-197) or harboring a BCR–ABL1 kinase domain mutation (samples 077 and 252). Samples with elevated FOXO1 expression are denoted by a red asterisk. (b) TKI-naive samples (180, 266 and 300) and patient samples with high FOXO1 (077, 109, 142, 185, 197 and 252) or low FOXO1 (123 and 186) were treated with dasatinib (50 nm) and/or GDC-0941 (300 nm) in colony-formation assays. The data represents percent of vehicle-treated controls. The error bars represent standard deviation. *P<0.05, ***P<0.001.