Table 1 Overview of published data on the potential role of MSPCs and derivates in the pathogenesis of MDS

▪Cytogenetic aberrations in MDS-MSPCs^{62, 63, 74}

▪Normal cytogenetics in MDS-MSPCs^{64, 66}

▪Lower expression of Dicer1, DROSHA,^{56, 57} AURKA, AURKB⁷⁵ genes in MDS-MSPCs

▪Normal structure, proliferation and differentiation potential of MDS-MSPCs^{62, 63, 64, 66}

▪Altered immunophenotype in MDS-MSPCs: decreased CD44 and CD49e,⁷⁰ CD90, CD104 and CD105⁶⁸ expression, increased CXCL12 expression⁷¹

▪Normal HSC support by MDS-MSPCs^{62, 63, 64}

▪Impaired proliferation and differentiation capacity of MDS-MSPCs^{58, 65, 70}

▪Impaired cytokine production, including IL-32, by MDS-MSPCs⁵⁸

▪Deregulation of Wnt signaling pathway in MDS-MSPCs^{82, 89}

▪Impaired HSPC support by MDS-MSPCs^{65, 66}