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. 2019 Apr 3;10:1519. doi: 10.1038/s41467-019-09469-3

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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. 5 — Hi-C of high hyperdiploid and ETV6/RUNX1-positive cases. a Contact matrices from chromosome 3, selected because it is disomic in all cases and displays no structural aberrations. The whole chromosome at 250 kb resolution is shown to the left and the 161–172 Mb region at 25 kb resolution to the right. At a resolution of 250 kb, the interaction profile is similar, showing that the general chromatin architecture is intact. However, at a resolution of 25 kb, it can clearly be seen that two of the high hyperdiploid cases (HeH_9 and HeH_10) have lost some topologically associating domains. b A/B compartment profile of chromosome 3 in cell line GM12878 and the six leukemia samples at 500 kb resolution. The profiles were similar between the cell line and the leukemias