Roles of CLU and the NF-κB pathway for HSC/MPPs of patients with untreated PV. (A) PV stem/progenitor cell protein signature. (B) Volcano plot of protein intensity fold changes and P values comparing HSC/MPP-specific findings of patients with untreated PV (PV.UT.HSC/MPP vs PV.UT.CMP/MEP) against HSC/MPP-specific findings of controls (Control.HSC/MPP vs Control.CMP/MEP), and (C) HSC/MPP-specific findings of PV patients with HU therapy (PV.HU.HSC/MPP vs PV.HU.CMP/MEP) against HSC/MPP-specific findings of patients with untreated PV (PV.UT.HSC/MPP vs PV.UT.CMP/MEP). (D) GSEA plot for NF-κB signaling in HSC/MPPs of patients with untreated PV compared with controls (PV.UT.HSC/MPP vs Control.HSC/MPP). The normalized enrichment score and significance values are provided. (E) Methylcellulose colony assay: Colony growth from FACS-isolated HSC/MPPs of patients with untreated chronic PV (PVchron.UT) was evaluated in the presence or absence of CLU, IKK-16, or their combination. Percentages of colonies relative to the total cell numbers plated are plotted. Error bars represent standard deviations. One-way (total colonies) and 2-way (granulocyte/macrophage and erythroid colonies) analysis of variance testing was applied using Tukey (1-way) and Dunnett (2-way) correction for multiple testing. *Adjusted P < .05; **adjusted P < .01; ***adjusted P < .001; ****adjusted P < .0001.