Figure 3.
SE-mediated drug resistance of malignant T cells is not limited to romidepsin. Representative flow cytometric plots (SS12 [A,C]; SS4 [E]; SS17 [G]; SS7 [I]) and quantifications of percentage of viable malignant cells from PBMCs of patients with SS cultured for 72 hours in the presence or absence of SE and treated with 1 μM vorinostat (A-B) (n = 5 [SS5, SS7, SS10, SS12, and SS17]), 2 μM resminostat (C-D) (n = 3 [SS4, SS10, and SS12]), 100 to 400 nM doxorubicin (E-F) (n = 4 [SS4, SS7, SS10, and SS17]; due to fluorescent properties of doxorubicin being incompatible with PI staining, we used Mitotracker red CMXRos to mark viable cells), 10 to 50 μM etoposide (G-H) (n = 5 [SS7, SS8, SS10, SS11, and SS17]), or 50 nM bortezomib (I-J) (n = 4 [SS7, SS10, SS11, and SS12]). Statistical significance was assessed by repeated measures 1-way ANOVA followed by Tukey multiple comparisons test. ∗P < .05; ∗∗P < .005; ∗∗∗P < .0005. DMSO, dimethyl sulfoxide; ns, not significant.

SE-mediated drug resistance of malignant T cells is not limited to romidepsin. Representative flow cytometric plots (SS12 [A,C]; SS4 [E]; SS17 [G]; SS7 [I]) and quantifications of percentage of viable malignant cells from PBMCs of patients with SS cultured for 72 hours in the presence or absence of SE and treated with 1 μM vorinostat (A-B) (n = 5 [SS5, SS7, SS10, SS12, and SS17]), 2 μM resminostat (C-D) (n = 3 [SS4, SS10, and SS12]), 100 to 400 nM doxorubicin (E-F) (n = 4 [SS4, SS7, SS10, and SS17]; due to fluorescent properties of doxorubicin being incompatible with PI staining, we used Mitotracker red CMXRos to mark viable cells), 10 to 50 μM etoposide (G-H) (n = 5 [SS7, SS8, SS10, SS11, and SS17]), or 50 nM bortezomib (I-J) (n = 4 [SS7, SS10, SS11, and SS12]). Statistical significance was assessed by repeated measures 1-way ANOVA followed by Tukey multiple comparisons test. ∗P < .05; ∗∗P < .005; ∗∗∗P < .0005. DMSO, dimethyl sulfoxide; ns, not significant.

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