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. 2018 Oct 15;119(10):1278–1287. doi: 10.1038/s41416-018-0232-5

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© The Author(s) 2018

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. 6 — Myc-proficient neuroblastoma cells are sensitive to C1A. a Growth inhibitory effect of C1A in a panel of neuroblastoma with different N-Myc expression. b Impact of HDAC6 inhibitors, C1A and tubastatin A, on caspase- 3/7 activity in SH-SY5Y and KELLY cells. Data are normalised by the amount of protein. Cells were treated for 24 h at the indicated concentration. c, d In vivo anti-tumour activity (c) of C1A and corresponding body weights (d) in KELLY mouse model of neuroblastoma. C1A was given twice daily at 20 mg/kg for 14 days (n = 3)