Figure 4
Figure 4. Apoptosis induction by ADI-PEG 20 in resistant and sensitive AML in vitro. ADI-PEG 20 induced apoptosis in half the AML samples in vitro. The expression of active caspase 3/7 following ADI-PEG 20 administration is shown in the ADI-sensitive (n = 19) and ADI-resistant AMLs (n = 19) as well as GMPB (n = 9) and normal hematopoietic stem cells (HSCs; n = 4) (A). Similar data were observed for annexin-V expression (B) for ADI-PEG 20–sensitive (n = 13) and ADI-PEG 20–resistant AML (n = 10) and GMPB (n = 7). (C) Cell death as defined by 4,6-diamidino-2-phenylindole staining was increased in sensitive AMLs (n = 13) but not resistant AML (n = 10), GMPB (n = 7), or normal HSCs (n = 4). Numbers of viable AML cells were reduced in ADI-PEG 20–sensitive AMLs (n = 19) but not ADI-PEG 20–resistant AML (n = 19) nor GMPB (n = 9) (D). *P < .05

Apoptosis induction by ADI-PEG 20 in resistant and sensitive AML in vitro. ADI-PEG 20 induced apoptosis in half the AML samples in vitro. The expression of active caspase 3/7 following ADI-PEG 20 administration is shown in the ADI-sensitive (n = 19) and ADI-resistant AMLs (n = 19) as well as GMPB (n = 9) and normal hematopoietic stem cells (HSCs; n = 4) (A). Similar data were observed for annexin-V expression (B) for ADI-PEG 20–sensitive (n = 13) and ADI-PEG 20–resistant AML (n = 10) and GMPB (n = 7). (C) Cell death as defined by 4,6-diamidino-2-phenylindole staining was increased in sensitive AMLs (n = 13) but not resistant AML (n = 10), GMPB (n = 7), or normal HSCs (n = 4). Numbers of viable AML cells were reduced in ADI-PEG 20–sensitive AMLs (n = 19) but not ADI-PEG 20–resistant AML (n = 19) nor GMPB (n = 9) (D). *P < .05

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