Figure 3.
ATRA upregulates CD38 expression on tumor cells and can enhance antitumor activity. (A) CD38 cell surface expression as measured by flow cytometry across the hematologic malignancies MM, AML, BL, and T-ALL after treatment with 10 nM of ATRA for 48 hours. (B) Mean fluorescence intensity (MFI) of CD38 expression on cell lines with and without ATRA treatment. (C) Cytotoxicity assays performed by coculturing WT and CD38-CAR NK cells against AML, MM, BL, and T-cell malignancies with and without 48-hour, 10-nM ATRA pretreatments. MM1S (n = 4), H929 (n = 4), AML-10 (n = 4), MV4-11 (n = 4), Raji (n = 4), Daudi (n = 4), and primary cells from patients with T-ALL (n = 3; mean ± SD). P values were calculated using a 2-way ANOVA; ∗P < .05; ∗∗ P <.01; ∗∗∗P = .001; ∗∗∗∗P < .0001.

ATRA upregulates CD38 expression on tumor cells and can enhance antitumor activity. (A) CD38 cell surface expression as measured by flow cytometry across the hematologic malignancies MM, AML, BL, and T-ALL after treatment with 10 nM of ATRA for 48 hours. (B) Mean fluorescence intensity (MFI) of CD38 expression on cell lines with and without ATRA treatment. (C) Cytotoxicity assays performed by coculturing WT and CD38-CAR NK cells against AML, MM, BL, and T-cell malignancies with and without 48-hour, 10-nM ATRA pretreatments. MM1S (n = 4), H929 (n = 4), AML-10 (n = 4), MV4-11 (n = 4), Raji (n = 4), Daudi (n = 4), and primary cells from patients with T-ALL (n = 3; mean ± SD). P values were calculated using a 2-way ANOVA; ∗P < .05; ∗∗ P <.01; ∗∗∗P = .001; ∗∗∗∗P < .0001.

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