Figure 1 Apoptotic destruction of... | American Society of Hematology

Figure 1

$Figure 1. Apoptotic destruction of primary B-precursor ALL cells and their in vivo clonogenic fraction by liposomal C61 nanoparticle (NP) formulation 25A. (A) Concentration-dependent apoptosis induction of primary LLPCs from patients with B-precursor ALL (N = 18) after treatment with 25A is shown. Treatment with 3 µg/mL 25A resulted in 70.5% ± 8.7% apoptosis, whereas 10 µg/mL caused 91.2% ± 3.8% apoptosis (P = .047) and 30 µg/mL caused 92.4% ± 2.4% apoptosis (P = .032). Neither drug-free control NP formulation 25B nor 2 Gy γ-rays caused a significant degree of apoptosis. In each of the 18 cases, there were at least 1 untreated control, 1 25B-treated control, and at least 1 test sample treated with 25A at 3, 10, or 30 µg/mL. Cumulatively, 0 µg/mL was tested in 18, 3 µg/mL in 11, 10 µg/mL in 12, and 30 µg/mL in 15 cases (see supplemental Methods). Ionizing radiation was tested in 9 cases based on the availability of the irradiator and specimen size. Cells were incubated with 25A or 25B for 24 hours in 2 cases, 48 hours in 13 cases, and 72 hours in 3 cases. (B) Concentration-dependent apoptosis induction of in vivo clonogenic LLPCs obtained from spleens of xenografted NOD/SCID mice challenged with primary LLPCs from 11 patients with B-precursor ALL after treatment with 25A is shown. In each of the 11 cases, there were at least 1 untreated control (in 9 cases there also was a 25B-treated control) and at least 1 test sample treated with 25A. Cumulatively, 0 µg/mL was tested in 11, 3 µg/mL in 5, 10 µg/mL in 5, and 30 µg/mL in 11 cases (see supplemental Methods). Ionizing radiation was tested in 5 cases based on the availability of the irradiator and sufficient cell numbers. Xenograft cells were incubated with 25A or 25B for 24 hours in 1 case, 48 hours in 9 cases, and 72 hours in 1 case. As in (A), neither drug-free control NP formulation 25B nor 2 Gy γ-rays caused a significant degree of apoptosis. SEM, standard error of the mean.$

Apoptotic destruction of primary B-precursor ALL cells and their in vivo clonogenic fraction by liposomal C61 nanoparticle (NP) formulation 25A. (A) Concentration-dependent apoptosis induction of primary LLPCs from patients with B-precursor ALL (N = 18) after treatment with 25A is shown. Treatment with 3 µg/mL 25A resulted in 70.5% ± 8.7% apoptosis, whereas 10 µg/mL caused 91.2% ± 3.8% apoptosis (P = .047) and 30 µg/mL caused 92.4% ± 2.4% apoptosis (P = .032). Neither drug-free control NP formulation 25B nor 2 Gy γ-rays caused a significant degree of apoptosis. In each of the 18 cases, there were at least 1 untreated control, 1 25B-treated control, and at least 1 test sample treated with 25A at 3, 10, or 30 µg/mL. Cumulatively, 0 µg/mL was tested in 18, 3 µg/mL in 11, 10 µg/mL in 12, and 30 µg/mL in 15 cases (see supplemental Methods). Ionizing radiation was tested in 9 cases based on the availability of the irradiator and specimen size. Cells were incubated with 25A or 25B for 24 hours in 2 cases, 48 hours in 13 cases, and 72 hours in 3 cases. (B) Concentration-dependent apoptosis induction of in vivo clonogenic LLPCs obtained from spleens of xenografted NOD/SCID mice challenged with primary LLPCs from 11 patients with B-precursor ALL after treatment with 25A is shown. In each of the 11 cases, there were at least 1 untreated control (in 9 cases there also was a 25B-treated control) and at least 1 test sample treated with 25A. Cumulatively, 0 µg/mL was tested in 11, 3 µg/mL in 5, 10 µg/mL in 5, and 30 µg/mL in 11 cases (see supplemental Methods). Ionizing radiation was tested in 5 cases based on the availability of the irradiator and sufficient cell numbers. Xenograft cells were incubated with 25A or 25B for 24 hours in 1 case, 48 hours in 9 cases, and 72 hours in 1 case. As in (A), neither drug-free control NP formulation 25B nor 2 Gy γ-rays caused a significant degree of apoptosis. SEM, standard error of the mean.

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