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. Author manuscript; available in PMC: 2011 Apr 29.
Published in final edited form as: Science. 2010 Mar 26;327(5973):1650–1653. doi: 10.1126/science.1186624

Figure 4. Deletion of β-catenin impairs the development of KLS-HoxA9/M and GMP-MLLAF9 induced AML.

Figure 4

a, GFP + cells in bone marrow of mice injected with floxed β-catenin (βcatloxp/loxp) or β-catenin-deficient (βcat−/−) KLS-HoxA9/M cells at 18 hr, 1 month, 4 months post-transplantation. HoxA9/M-βcatloxP/loxP KLS cells were transduced with a retroviral vector encoding Cre recombinase to generate βcat −/− KLS-HoxA9/M cells or an empty vector to generate control βcatloxp/loxp KLS-HoxA9/M cells. After selection, 1 × 106 infected cells were transplanted into sublethally irradiated recipients (n=5 in each group). Mice were sacrificed at the indicated time points to assess for GFP+ cells.

b, Survival curves of mice transplanted with βcat−/− KLS-HoxA9/M cells, βcatloxp/loxp KLS-HoxA9/M cells, and empty vector or Cre-infected WT KLS-HoxA9/M (KLS cells were sorted from wild-type C57BL/6 mice and transformed with HoxA9/M to assess the effect of Cre on KLS-HoxA9/M leukemia development; n=10 for each group).

c, Survival curves of mice transplanted with βcat−/− GMP-MLLAF9 cells and βcatloxp/loxp GMP-MLLAF9 cells (n=10 for each group). P determined using the log-rank test