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. 2019 Nov 28;10:5428. doi: 10.1038/s41467-019-13315-x

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© The Author(s) 2019

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 3 — PIM1 inhibition lacks potency but enhances the efficacy of ALK inhibitors. a RT-qPCR-based expression levels of PIM1 in 25 neuroblastoma cell lines, normalized to GIMEN cell line expression levels. Data represent means ± s.d. of technical triplicates. b 14-day colony formation assay of ALK-positive NB cell lines treated with the indicated doses of AZD1208. c 72-h dose–response assays of ALK-positive NB cell lines treated with AZD1208 or PIMi. Data represent means ± s.d. of technical triplicates. d, e Analysis of PIM1 levels by RT-qPCR in d CHLA-20 or e KELLY cells with shRNA-mediated knockdown of PIM1. NT, non-targeting. Data represent means ± s.d. of triplicate experiments. f, g 72-h dose–response assays following brigatinib or ceritinib exposure in f CHLA-20 cells or g KELLY cells treated with PIM1-targeting or NT shRNA. Data points represent means ± s.d. of duplicate f or triplicate g experiments. ED₅₀ values were compared by an unpaired Student’s t-test. Source data for 3a and 3d-g are provided as a Source Data file.