Figure 7.
ChT-1A5 in combination with NK cells inhibits tumor growth via antibody-dependent cellular cytotoxicity in AML PDX model. (A) Experimental design. Two million AML PDX cells were injected into NSG mice via the TV. After 1 week, mice were treated with ChT1A5 or rituximab at 1 mg/kg twice weekly via IP injections and with NK cells (10 × 106) via TV twice weekly. (B) AML PDX growth in mouse PB. Mouse blood samples were analyzed weekly for human CD45+ cells by flow cytometry. When human CD45+ cells reached >95% or when mice became moribund (whichever occurred first), mice were killed. (C) Bodyweight of leukemia-bearing mice treated with ChT-1A5 or rituximab and NK cells; weight was measured once a week. (D) Kaplan-Meier survival plot representing OS rates in mice treated with ChT-1A5 or rituximab and NK cells.

ChT-1A5 in combination with NK cells inhibits tumor growth via antibody-dependent cellular cytotoxicity in AML PDX model. (A) Experimental design. Two million AML PDX cells were injected into NSG mice via the TV. After 1 week, mice were treated with ChT1A5 or rituximab at 1 mg/kg twice weekly via IP injections and with NK cells (10 × 106) via TV twice weekly. (B) AML PDX growth in mouse PB. Mouse blood samples were analyzed weekly for human CD45+ cells by flow cytometry. When human CD45+ cells reached >95% or when mice became moribund (whichever occurred first), mice were killed. (C) Bodyweight of leukemia-bearing mice treated with ChT-1A5 or rituximab and NK cells; weight was measured once a week. (D) Kaplan-Meier survival plot representing OS rates in mice treated with ChT-1A5 or rituximab and NK cells.

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