Figure 4
Trib1 and Evi1 accelerate the onset of Hoxa9/Meis1-AML. (A-B) Leukemia- and disease-free survival of animals was compared. Kaplan-Meier survival curves are shown for Trib1 (n = 12), Trib1/Hoxa9/Meis1 (n = 12), and Hoxa9/Meis1 + pMYs-GFP (n = 8) (A). The same analysis was performed for Evi1 (n = 8), Evi1/Hoxa9/Meis1 (n = 8), and Hoxa9/Meis1 + pMYs-GFP (n = 8) (B), although single infection of the Evi1 retrovirus did not induce AML but did induce death due to severe anemia as a result of MDS. (C) Integrations of each retrovirus were confirmed by Southern blotting. Leukemia DNAs were digested with EcoRV and hybridized with GFP (for Trib1 and Evi1 retroviruses) and Hoxa9 probes. N indicates the liver DNA of the normal C57Bl/6J mouse; and *, the endogenous Hoxa9 signal.

Trib1 and Evi1 accelerate the onset of Hoxa9/Meis1-AML. (A-B) Leukemia- and disease-free survival of animals was compared. Kaplan-Meier survival curves are shown for Trib1 (n = 12), Trib1/Hoxa9/Meis1 (n = 12), and Hoxa9/Meis1 + pMYs-GFP (n = 8) (A). The same analysis was performed for Evi1 (n = 8), Evi1/Hoxa9/Meis1 (n = 8), and Hoxa9/Meis1 + pMYs-GFP (n = 8) (B), although single infection of the Evi1 retrovirus did not induce AML but did induce death due to severe anemia as a result of MDS. (C) Integrations of each retrovirus were confirmed by Southern blotting. Leukemia DNAs were digested with EcoRV and hybridized with GFP (for Trib1 and Evi1 retroviruses) and Hoxa9 probes. N indicates the liver DNA of the normal C57Bl/6J mouse; and *, the endogenous Hoxa9 signal.

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