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. 2015 Sep 7;6(32):33206–33216. doi: 10.18632/oncotarget.5091

Figure 5. Effects of PIM kinase inhibition on primary leukemic progenitors from CML patients.

Figure 5

A. Primary mononuclear cells derived from CML patient samples were plated in methylcellulose in the presence of control (DMSO) or SGI-1776 at the indicated concentrations for approximately fourteen days. Leukemic progenitor colony formation (CFU-GM) was assessed in clonogenic assays in methylcellulose. Data are expressed as a percentage of DMSO control-treated cells. Shown are the means + SE of five experiments performed with samples from five different patients. ***p < 0.001 using a paired t-test. B. Primary mononuclear cells derived from CML patient samples were plated in methylcellulose in presence of control (DMSO), SGI-1776 (0.5 μmol/L) or imatinib (0.5 μmol/L) alone or in combination for approximately fourteen days, as indicated. Leukemic progenitor colony formation (CFU-GM) was assessed in clonogenic assays in methylcellulose. Data are expressed as a percentage of DMSO control-treated cells. Shown are the means + SE of five experiments performed with samples from five different patients. *p < 0.05, **p < 0.01, ***p < 0.001 using a paired t-test C. Primary mononuclear cells derived from CML patient samples were plated in methylcellulose in the presence of control (DMSO) or AZD-1208 at the indicated doses for approximately fourteen days. Leukemic progenitor colony formation (CFU-GM) was assessed in clonogenic assays in methylcellulose. Data are expressed as a percentage of DMSO control-treated cells. Shown are the means + SE of four experiments performed with samples from four different patients. **p < 0.01 using a paired t-test.