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. 2019 Jul 22;11:106. doi: 10.1186/s13148-019-0704-3

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© The Author(s). 2019

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 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.

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Fig. 2 — Mutation spectrum and response to guadecitabine. a Association of mutation spectrum, clinical characteristics, and response to guadecitabine in r/r AML (n = 122). Genomic mutation analysis was performed using the TruSight Myeloid Sequencing Panel (Illumina). The gene rows in the graph represent individual genomic lesions, the clinical characteristics row represent simplified clinical information, and the columns represent patients in the study. Black in the gene row indicates the presence of a specified mutation in a patient, and colors in the clinical characteristics row represent low (blue) to high (red). b Comparison of the mutation rate of CR vs. non-CR patients. None of the genes showed a significant correlation with CR, but there was a strong trend for RAS mutations (N or K) to be associated with resistance to guadecitabine (CR were seen in 0/22 patients with RAS mutations compared to 15/100 patients without RAS mutations, p = 0.07). c Kaplan-Meier survival analysis stratified by RAS mutation status. The presence of RAS mutations was associated with a significantly worse survival (p = 0.0004 by log-rank test)