Dasatinib enhances apoptosis and inhibits cell proliferation in combination with chemotherapeutic agents in AML primitive and committed progenitors. AML CD34⁺ cells were labeled with CFSE, cultured for 72 hours either with dasatinib alone (200 nM), DNR alone (50 nM), or dasatinib (dasatinib 200 nM) in combination with DNR (A) or with Ara-C alone (50 nM) or dasatinib in combination with Ara-C (B). PI was determined using ModFit software, and proliferation indices were normalized to untreated controls. Histograms showing mean ± SEM for proliferation of 5 AML is shown (left), and a representative CFSE cytometry flow plot indicating the calculated PI index is also shown (right). One-way ANOVA with posttest: ns, nonsignificant; *P < .0465; **P < .001; ***P < .003; ****P < .0001. (C) Apoptosis of AML samples (n = 6) cultured for 72 hours with dasatinib alone (200 nM), DNR alone (50 nM), Ara-C alone (50 nM), or dasatinib (dasatinib 200 nM) in combination with DNR (left) and Ara-C (right). Results shown are presented as mean ± SEM of Annexin V-positive cells for 6 AML samples. One-way ANOVA with posttest: ns, nonsignificant; *P < .05; ****P < .0001. (D) CFC generated from AML cells exposed for 48 hours to dasatinib alone (200 nM), DNR alone (10 and 50 nM; left, n = 6), Ara-C alone (10 and 50 nM; right, n = 5), or dasatinib in combination with DNR (left, n = 6) and Ara-C (right, n = 5). One-way ANOVA with posttest: *P < .05; ****P < .0001. Results shown are presented as percentage of control (mean ± SEM).