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. 2016 Oct 25;7(48):79637–79653. doi: 10.18632/oncotarget.12876

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Copyright: © 2016 Boi et al.

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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A. Phosphorylation levels of NPM-ALK in control (wild type NPM-ALK) and C1156Y NPM-ALK mutated transfected TS-Supm2 cells treated with a range of doses of CEP28122, according to Western blotting. β-actin was used as a loading control. NT, not treated control cells B. Percent cell death in cells (TS-Supm2, NPM-ALK wild type transfected, C1156Y-mutated) treated with CEP28122 at a range of concentrations for increasing exposure times (12, 24, 48 h) according to qRT-PCR. C. Combination treatment with OTX015 (250 nM) and CEP28122 (50 nM) in cells overexpressing wild type or NPM-ALK C1156Y mutation did not rescue drug resistance according to qRT-PCR. D. GANT61 and OTX015 combination treatment overcomes the resistance associated with the overexpression of wild type NPM-ALK or the C1156Y NPM-ALK mutated form.

A. Phosphorylation levels of NPM-ALK in control (wild type NPM-ALK) and C1156Y NPM-ALK mutated transfected TS-Supm2 cells treated with a range of doses of CEP28122, according to Western blotting. β-actin was used as a loading control. NT, not treated control cells B. Percent cell death in cells (TS-Supm2, NPM-ALK wild type transfected, C1156Y-mutated) treated with CEP28122 at a range of concentrations for increasing exposure times (12, 24, 48 h) according to qRT-PCR. C. Combination treatment with OTX015 (250 nM) and CEP28122 (50 nM) in cells overexpressing wild type or NPM-ALK C1156Y mutation did not rescue drug resistance according to qRT-PCR. D. GANT61 and OTX015 combination treatment overcomes the resistance associated with the overexpression of wild type NPM-ALK or the C1156Y NPM-ALK mutated form.