Fig. 1.
Fig. 1. Dose-response curves of the inhibition of proliferation of CFU-GM, BFU-E, and CFU-GEMM by Exodus-1, Exodus-2, and Exodus-3. / Progenitor assays of marrow from 2 newly diagnosed, untreated patients with chronic myelogenous leukemia (CML) were performed with varying concentrations of the Exodus chemokines. MIP-1α served as a negative control and did not inhibit CFU-GM proliferation to any appreciable extent, even at concentrations of up to 500 ng/mL. Data are presented as the average of the percentage of proliferative inhibition from triplicate cultures compared with control average colony formation without chemokine treatment. Mean (± SD) control colonies were 22 ± 3 for CFU-GM, 126 ± 14 for BFU-E, and 13 ± 3 for CFU-GEMM for CML patient 1 and 195 ± 10 for CFU-GM, 168 ± 10 for BFU-E, and 49 ± 5 for CFU-GEMM for CML patient 2.

Dose-response curves of the inhibition of proliferation of CFU-GM, BFU-E, and CFU-GEMM by Exodus-1, Exodus-2, and Exodus-3.

Progenitor assays of marrow from 2 newly diagnosed, untreated patients with chronic myelogenous leukemia (CML) were performed with varying concentrations of the Exodus chemokines. MIP-1α served as a negative control and did not inhibit CFU-GM proliferation to any appreciable extent, even at concentrations of up to 500 ng/mL. Data are presented as the average of the percentage of proliferative inhibition from triplicate cultures compared with control average colony formation without chemokine treatment. Mean (± SD) control colonies were 22 ± 3 for CFU-GM, 126 ± 14 for BFU-E, and 13 ± 3 for CFU-GEMM for CML patient 1 and 195 ± 10 for CFU-GM, 168 ± 10 for BFU-E, and 49 ± 5 for CFU-GEMM for CML patient 2.

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