Figure 4
Figure 4. Effect of bortezomib treatment on quiescent CD34+ and cycling CD34+ and CD34− CML cells. (A) Enhancement of killing of quiescent CD34+ CML cells (QSC), but not cycling CD34+ (CD34+DIV) or CD34− (CD34NEG) cells following bortezomib treatment. AUTO = autologous control (B) Anti-TRAIL antibody diminishes the enhanced NK-cell cytotoxicity of QSC following bortezomib treatment. Bortezomib treatment versus no treatment, P = .019; bortezomib treatment with anti-TRAIL antibody versus no treatment, P = .448, at 20:1 E/T ratio, using Welch modified 2-sample t test. (Data using cells from UPI 481, blast-crisis CML; 16-hour cytotoxicity using expanded HLA-identical donor NK cells, representative of cytotoxicity assays from 3 separate patient-donor pairs, n = 2 accelerated-phase, n = 1 blast-crisis CML.)

Effect of bortezomib treatment on quiescent CD34+ and cycling CD34+ and CD34 CML cells. (A) Enhancement of killing of quiescent CD34+ CML cells (QSC), but not cycling CD34+ (CD34+DIV) or CD34 (CD34NEG) cells following bortezomib treatment. AUTO = autologous control (B) Anti-TRAIL antibody diminishes the enhanced NK-cell cytotoxicity of QSC following bortezomib treatment. Bortezomib treatment versus no treatment, P = .019; bortezomib treatment with anti-TRAIL antibody versus no treatment, P = .448, at 20:1 E/T ratio, using Welch modified 2-sample t test. (Data using cells from UPI 481, blast-crisis CML; 16-hour cytotoxicity using expanded HLA-identical donor NK cells, representative of cytotoxicity assays from 3 separate patient-donor pairs, n = 2 accelerated-phase, n = 1 blast-crisis CML.)

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