Fig. 7: The collaboration of DNMT3A-MT with Kmt2a-PTD shows shorter latency in vivo. | Oncogenesis

Fig. 7: The collaboration of DNMT3A-MT with Kmt2a-PTD shows shorter latency in vivo.

From: DNMT3A mutants provide proliferating advantage with augmentation of self-renewal activity in the pathogenesis of AML in KMT2A-PTD-positive leukemic cells

Fig. 7

a Kaplan−Meier curve shows the survival of mice transplanted with BM cells harboring Kmt2a and transduced with empty vector (EV, n = 5) control, DNMT3A-WT, DNMT3A-R882C/H/S (n = 5). P values were calculated using a log-rank test. b, c Quantification of hepatomegaly (b) and splenomegaly (c) in mice transduced with EV, DNMT3A-WT, DNMT3A-R882C/H/S were shown (n = 5). d−f Peripheral blood counts of transduced mice were shown (n = 5 for each group). *P < 0.05, **P < 0.01, ***P < 0.005, compared with the DNMT3A-WT group.

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