. Author manuscript; available in PMC: 2022 Nov 1.

Published in final edited form as: Arterioscler Thromb Vasc Biol. 2021 Oct 7;41(11):2661–2670. doi: 10.1161/ATVBAHA.121.316373

Table 2.

Summary of cell types for transcriptomic study in MPNs, study findings, advantages and disadvantages of each source.

Cell type	MPN subtypes	Findings
Whole blood¹²¹	Healthy donors, ET, PV, MF	• Dysregulation of genes involved in inflammation • Detects signatures that might be missed by profiling isolated cell types
Granulocytes¹²²	Healthy donors, ET, PV, MF	• JAK-STAT signature common across disease sub-types and driver mutations • TET2 mutation is associated with a distinct signature • Extent of clonal predominance may influence signatures
Circulating stem and progenitor cells¹²³	JAK2V617F mutated PV	• Reveals heterogeneity, separates patients into distinct groups with different rates of disease complications • Rare cell type, may not be sufficiently abundant in all MPN subtypes
Circulating stem and progenitor cells¹⁵	MF, mobilised cells in healthy donors	• Heterogeneity of Mk progenitors in MF cell type, cost if performing single cell sequencing
Platelets¹²⁴	ET, reactive thrombocytosis	• Transcript profiles distinguish ET from reactive thrombocytosis
Platelets¹⁰⁶	Healthy donors, MF	• Distinguishes MF from controls, separates patients into groups with and without fibrosis
Platelets^{12, 104}	Healthy donors, ET, PV, MF	• Two mutually validating MPN patient RNA-seq cohorts discriminate each clinical phenotype; and identify progressive transcriptomic markers that also enable predictive signatures for MF.