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. 2021 Jan 28;13:21. doi: 10.1186/s13148-021-01011-x

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© The Author(s) 2021

Open AccessThis 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/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 6 — a Circos plot including driver mutation associations among 65 AML patients. Colors are determined by functional pathway of each given gene. b Patterns of association of mutations among studied patients. MLL mutations also include MLL-MLLT3 and MLL-MLLT4 fusion gene lesions while KMT2A represents KMT2A specific gene lesions only. c Patterns of association of mutational pathway abnormalities among studied patients. d Patterns of association of mutations among ASXL1, BCOR, U2AF1, SRSF2 patients with significantly lower H3K27me3 levels than wildtype. Filled areas represent significant positive (red) or negative (blue) co-occurrence p < 0.05. Color and size indicate of filled area indicates Pearson’s correlation coefficient