FigureĀ 4.
Mass cytometry analysis shows combination ATRA and CD38-CAR NK-cell treatment decreases live AML population. Mass cytometry analysis was performed 24 hours after the coculture of a primary AML cell line (AML-1) with WT or CD38-CAR NK cells with and without 48-hour, 10-nM ATRA pretreatment. Eight distinct conditions were analyzed: WT NK cells alone (A), CD38-CAR NK cells alone (B), AML cells alone (C), AML plus WT NK cells (D), AML plus CD38-CAR NK cells (E), AML cells with ATRA (F), AML plus ATRA plus WT NK cells (G), and AML plus ATRA plus CD38-CAR NK cells (H). (I) Heat map of surface marker appearing on the live AML cells after treatment analyzed by mass cytometry. Original values are ln(x)-transformed. Rows are centered; unit variance scaling is applied to rows. Both rows and columns are clustered using correlation distance and average linkage using ClustVis.

Mass cytometry analysis shows combination ATRA and CD38-CAR NK-cell treatment decreases live AML population. Mass cytometry analysis was performed 24 hours after the coculture of a primary AML cell line (AML-1) with WT or CD38-CAR NK cells with and without 48-hour, 10-nM ATRA pretreatment. Eight distinct conditions were analyzed: WT NK cells alone (A), CD38-CAR NK cells alone (B), AML cells alone (C), AML plus WT NK cells (D), AML plus CD38-CAR NK cells (E), AML cells with ATRA (F), AML plus ATRA plus WT NK cells (G), and AML plus ATRA plus CD38-CAR NK cells (H). (I) Heat map of surface marker appearing on the live AML cells after treatment analyzed by mass cytometry. Original values are ln(x)-transformed. Rows are centered; unit variance scaling is applied to rows. Both rows and columns are clustered using correlation distance and average linkage using ClustVis.

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