Fig. 1: Epigenomic analysis of AML patient data reveals NUP98 fusion-specific patterns. | Nature Communications

Fig. 1: Epigenomic analysis of AML patient data reveals NUP98 fusion-specific patterns.

From: Transcriptional and epigenetic rewiring by the NUP98::KDM5A fusion oncoprotein directly activates CDK12

Fig. 1

A Principal component (PC) analysis of ATAC-seq data from pediatric and adult AML patients and samples from healthy blood cells, including HSCs, progenitor cells, and mature myeloid cells. B Minimum spanning tree of distances between ATAC-seq signals of NUP98 fusion-expressing and other pediatric AML samples and samples of healthy blood cells. C ATAC-seq profile plots showing 1921 more accessible regions in NUP98 fusion-expressing AML vs. GMPs. D Heatmap and profile plots of ATAC-seq, H3K27ac, and H3K4me3 CUT&Tag data showing 1921 genomic regions that are more accessible in NUP98 fusion-expressing AML vs. GMPs. E Heatmap showing ATAC-seq unsupervised clustering of 893 differentially accessible regions in NUP98 fusion-expressing AML patient samples compared to NUP98 wild-type pediatric AML patient samples (HSC hematopoietic stem cell, MPP multipotent progenitor, CMP common myeloid progenitor, MEP Megakaryocyte-erythrocyte progenitor, GMP granulocyte-monocyte progenitor). Source data are provided as a Source Data file.

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