Fig. 1: The landscape of MPN/sAML CD34 + HSPCs.

a Oncoprint of MPN/sAML samples in the WashU Cohort CD34 + RNA-seq. b Comparison of genetic alterations in WashU sAML (n = 34) and additional non-myeloproliferative neoplasm AML cohorts, TCGA (n = 200) and BeatAML2 (n = 893). c Schematic of the WashU Cohort CD34 + RNA-seq encompassing 90 primary samples representative of PV (n = 6), ET (n = 9), MF (n = 30), sAML (n = 34) and NBM (n = 11). d Principal component analysis of primary samples in the WashU Cohort CD34 + RNA-seq by gene expression. e Boxplots showing expression of key genes mediating oncogenic signaling through the mTOR/PI3K/AKT and receptor tyrosine kinase/RAS/RAF pathways across the WashU Cohort by disease. Statistics assessed by a two-tailed student’s t test. † denotes the comparison between MF and NBM. ‡ denotes the comparison between sAML and NBM. Sample numbers are denoted in panel (c). Boxplot showing median, upper, and lower quartiles with whiskers representing highest and lowest values excluding outliers, and potential outliers. f Schematic of mass cytometry analysis of CD34 + cells from the WashU Cohort encompassing 106 primary samples representative of PV (n = 17), ET (n = 5), MF (n = 34), sAML (n = 15) and normal healthy donors (n = 35). g Left: Heatmap of phosphorylated and total protein expression by mass cytometry. Values from patient samples were normalized to values from the normal control from each CyTOF run and are denoted as 90th percentile arcsinh ratios. Right: Boxplots showing phosphorylation of key protein by disease. Statistics assessed by a two-tailed student’s t test. † denotes the comparison between MF and NBM. ‡ denotes the comparison between sAML and NBM. Sample numbers are denoted in panel (f). Boxplot showing median, upper, and lower quartiles with whiskers representing highest and lowest values excluding outliers, and potential outliers.