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. 2021 Mar 31;11:7288. doi: 10.1038/s41598-021-86646-9

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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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.

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Pediatric AML patients with cohesin mutations have a transcriptomic signature which indicates they may be responsive to DOT1L inhibition. (a) Heatmap illustrating the clustering of cohesin-mutated patients (10 patients, 4 with primary and relapsed diseased, for a total of 14 samples) and cohesin-WT patients (49 patients). (b) Box and Whisker plots comparing TARGET AML expression data across the HOXA locus in cohesin mutant (n = 14) versus cohesin-WT (n = 49). According to the Wilcox test, significance is not reached for any gene. (C) GSEA analysis showing enrichment for a DOT1L inhibitor-derived signature.