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. 2019 Nov 20;9:17213. doi: 10.1038/s41598-019-53610-7

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© The Author(s) 2019

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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NP23-NHD13 AML gene expression profile is distinct from single transgenic NP23 and NHD13 AML. (a) PCA plot derived from NP23, NHD13 and NP23-NHD13 AML (all BM samples) compared to WT Lin⁻ BM. (b) Hierarchical clustering shows NP23-NHD13 leukemia samples cluster distinct from WT, NP23 and NHD13 leukemia samples. (c) Venn diagram indicates 76 genes differentially expressed in NP23-NHD13 AML. (d) GSEA comparison of genes differentially (defined as 2-fold expression change, p < 0.05) expressed between NP23-NHD13 AML and WT LN BM demonstrates that gene sets upregulated in NP23-NHD13 AML are also enriched in specific human AML gene sets, (e) Enrichment of genes overexpressed in NP23-NHD13 AML correlate with genes enriched in normal human myeloid development.