Figure 1.
Aberrant phenotypic LSCs can be detected before the onset of sAML/sMDS. Flow cytometric analysis was conducted on collected stem and progenitor cells from patients who later developed sAML/sMDS and from mobilized controls. Patient samples demonstrated a decrease in total HSPCs (Lin− CD34+ CD38−) (A-B), a decrease in CMPs (Lin−, CD34+, CD38+, CD123+, CD45ra−) (C-D), a decrease in healthy HSPCs (Lin−, CD34+, CD38−, CD123−, CD45ra−) (E-F), and a trend toward an increase in CD123+ HSPCs (Lin−, CD34+, CD38−) (G-H). These effects were most pronounced in patient 3, who developed sAML shortly after specimen collection. Means and standard deviations for stem and progenitor populations are depicted as frequencies of parental population (top of FACS plots: panels A, C, E, and G; and y-axes: panels B, D, F, and H). Student t test: *P < .05. n.s., not significant.

Aberrant phenotypic LSCs can be detected before the onset of sAML/sMDS. Flow cytometric analysis was conducted on collected stem and progenitor cells from patients who later developed sAML/sMDS and from mobilized controls. Patient samples demonstrated a decrease in total HSPCs (Lin CD34+ CD38) (A-B), a decrease in CMPs (Lin, CD34+, CD38+, CD123+, CD45ra) (C-D), a decrease in healthy HSPCs (Lin, CD34+, CD38, CD123, CD45ra) (E-F), and a trend toward an increase in CD123+ HSPCs (Lin, CD34+, CD38) (G-H). These effects were most pronounced in patient 3, who developed sAML shortly after specimen collection. Means and standard deviations for stem and progenitor populations are depicted as frequencies of parental population (top of FACS plots: panels A, C, E, and G; and y-axes: panels B, D, F, and H). Student t test: *P < .05. n.s., not significant.

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