Figure 2. Effects of tyrosine kinase inhibitors on myeloid differentiation. (A–D). Human acute myeloid leukemia HL-60 cells were treated with 10 μM erlotinib (ERLO, E), 10 μM gefitinib (GEFI), 100 nM dasatinib (DASA), 5 μM lapatinib (LAPA), 5 μM imatinib (IMA), 5 μM sorafenib (SORA), 500 nM nilotinib (NILO), 500 nM sunitinib (SUNI), or an equal volume of DMSO, alone or combined with 100 nM all-trans retinoic acid (ATRA) or 50 nM 1α,25-hydroxycholecalciferol (VD), for 3 d, and then processed for the cytofluorometry-assisted detection of CD11b (A–C) or CD14 (B–D) expression. Panels (Aand B) report representative CD11b and CD14 expression profiles, respectively. ISO, isotype control. Panels (C and D) illustrate quantitative data on the percentage of CD11b- and CD14 -expressing cells, respectively (means ± SEM; n = 2–3). *P < 0.05, **P < 0.01, ***P < 0.001 (ANOVA plus Dunnett post-hoc test) as compared with DMSO-treated cells; ###P < 0.001 (ANOVA plus Bonferroni post-hoc test), as compared with ATRA-treated cells; +P < 0.05, ++P < 0.01 +++P < 0.001 (ANOVA plus Bonferroni post-hoc test), as compared with VD-treated cells.