Fig. 2: Asciminib retains potent antileukemic activity in secondary transplants. | Leukemia

Fig. 2: Asciminib retains potent antileukemic activity in secondary transplants.

From: Asciminib antagonizes transplantable BCR::ABL1-positive lymphoid blast crisis in vivo by targeting malignant stem cells

Fig. 2

A Percentage of B220 medium-high (med-high) cells in peripheral blood, bone marrow, and spleen of the secondary transplantations were analyzed by flow cytometry. Colors indicate the treatment in the first transplant. B Peripheral blood, bone marrow, and spleen were analyzed by flow cytometry for the B lymphoblastic population, and vehicle-treated mice were divided into the treatment groups of the first transplant and illustrated in a box-and-whisker plot with highlighted median. C BCR::ABL1 expression, normalized to Gapdh, in the spleen of transplanted mice. For (AC), Mann–Whitney-U-test was performed. D Overview of mutations found in the kinase domain and myristoyl binding site (aa 268–540) of BCR::ABL1 in secondary transplantations of SCL tTA-BCR::ABL1 mice. The mutations which were detected were assorted into four groups, depending on the treatment of first and secondary recipients, and again into three subgroups, comprising already described mutations in BCR::ABL1 (violet; partly known to provide TKI resistance), previously described mutations of unknown significance in ABL1 (dark red), and undescribed, novel mutations (black) of unknown significance in the kinase domain and myristoyl binding site of BCR::ABL1. aa amino acid, VEH vehicle.

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