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. 2021 Jul 1;35(10):2978–2982. doi: 10.1038/s41375-021-01333-y

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© The Author(s) 2021

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. 2 — a Pie diagrams with the proportions of different NUTM1 partner genes among infants (N = 39; left) and children from the age of 1 (N = 32; right) with a known fusion partner. Below the pie diagrams, each patient is represented by a dot color-coded for the fusion, depicted along age at diagnosis (x-axis) for infants (in months; left) and children (in years; right) and gender (y-axis). Dots are plotted with a small offset to avoid overlap. b Dot plot showing NUTM1 and HOXA9 expression. Infant cases (N = 19; left panel) are indicated by a circle, pediatric cases (N = 19; right panel) by a diamond. Ten infants and nine children with B-ALL without NUTM1 or KMT2A rearrangement were included as controls (gray). Counts from RNA-sequencing libraries were normalized to fragments per kilobase per million (FPKM), 0 was substituted by 0.005, subsequently FPKM values were log10-transformed. The median HOXA9 expression across all 57 samples was 0.85 FPKM (log10 value–0.073), indicated by the dotted line.