Figure 3.
Evidence of residual disease in the splenic niche of ETP-ALL PDX. (A) As shown, 2 × 106 cells of PDX-1 were injected in the tail vein of male NSG mice until the engraftment of human CD45+ cells. The animals were then randomized into vehicle and ABT-199 treatment (25 mg/kg by oral gavage daily) groups. (B) Percentage of hCD45+ blasts in the peripheral blood upon treatment. (C) Percentage of hCD45+ blasts in the blood, bone marrow, and spleen of vehicle- and ABT-199–treated mice at the end of 21 and 36 days. (D) BH3 profile of hCD45+ cells isolated from bone marrow and spleen of PDX-1 mouse models. (E-G) BH3 profile of hCD45 blasts isolated from the blood, bone marrow, and spleen of T-ALL PDX-2, PDX-3, and PDX-4 mouse models. Mean ± SEM; n = 3. Two-way analysis of variance with Bonferroni multiple comparison test was used to calculate statistical significance. *P < .05, **P < .01, ****P < .0001.

Evidence of residual disease in the splenic niche of ETP-ALL PDX. (A) As shown, 2 × 106 cells of PDX-1 were injected in the tail vein of male NSG mice until the engraftment of human CD45+ cells. The animals were then randomized into vehicle and ABT-199 treatment (25 mg/kg by oral gavage daily) groups. (B) Percentage of hCD45+ blasts in the peripheral blood upon treatment. (C) Percentage of hCD45+ blasts in the blood, bone marrow, and spleen of vehicle- and ABT-199–treated mice at the end of 21 and 36 days. (D) BH3 profile of hCD45+ cells isolated from bone marrow and spleen of PDX-1 mouse models. (E-G) BH3 profile of hCD45 blasts isolated from the blood, bone marrow, and spleen of T-ALL PDX-2, PDX-3, and PDX-4 mouse models. Mean ± SEM; n = 3. Two-way analysis of variance with Bonferroni multiple comparison test was used to calculate statistical significance. *P < .05, **P < .01, ****P < .0001.

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