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. 2018 Jul 26;8:11293. doi: 10.1038/s41598-018-29593-2

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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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Log2 expression values for the three genes selected as mediators both for the RUNX1+ vs. RUNX1− comparison and the t(8; 21)+ vs. t(8; 21)− comparison. Log2 expression values in AMLCG Cohort 1 (panel a) and AMLCG Cohort 2 with TCGA (panel b) for the three genes that appear in both, Supplementary Tables S1 and S2, separated by whether only mutations (RUNX1+), only fusion (t(8; 21)+) or neither of these two (RUNX1− and t(8; 21)−) are present in the respective patients. The p values are the results of Wilcoxon tests. For each gene, we tested ‘RUNX1+’ against ‘RUNX1− and t(8; 21)−’ and ‘t(8; 21)+’ against ‘RUNX1− and t(8; 21)−’.