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. 2012 Oct 22;209(11):2017–2031. doi: 10.1084/jem.20121343

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© 2012 Thiollier et al.

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Figure 7. — Aurora kinase inhibitors inhibit proliferation of AMKL patient blasts in vitro. (A) AMKL7 cells purified from immunodeficient recipients were cultured in vitro in the presence of DMSO (control), 5 µM DiMF, or 250 nM MLN8237 for 72 h. A representative flow cytometry analysis of CD41 and CD42 megakaryocyte–specific markers is shown. (B) Histogram representation of CD41⁺CD42⁺ maturing megakaryocyte elements shown in A. (C) Representative ploidy analysis of cells treated as in A. (D) Histogram representation of cells with a ploidy > 4n shown in C. (E) Representative apoptosis analysis of cells treated as in A. (F) Histogram representation of apoptotic cells (AnnexinV⁺7AAD⁻ cells) shown in E. (G) Representative flow cytometry analysis of cleaved caspase 3 in cells treated as in A. (H) Histogram representation of cleaved caspase 3–positive cells shown in G. (B, D, F, and H) Mean value ± SEM of duplicate (B and D) or triplicate (F and H) experiments is shown. (I) Proliferation of AMKL7 leukemic cells upon treatment with aurora kinase inhibitors. Mean ± SEM of the number of viable cells (trypan blue exclusion, duplicate experiments) is shown. (J) Effect of 5 µM DiMF and 250 nM MLN8237 treatment on AMKL1 cells. Flow cytometry analysis of ploidy and differentiation after 6 d of in vitro treatment. (K) Effect of 5 µM DiMF and 250 nM MLN8237 treatment on AMKL4 cells. Flow cytometry analysis of ploidy and differentiation after 4 d of in vitro treatment. (L) Viable number of AMKL4 cells after 4 d of treatment as in K. Means ± SEM of duplicate experiments are shown.