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. 2019 Mar 19;216(4):966–981. doi: 10.1084/jem.20181276

Figure 3.

Figure 3.

Ezh2 functions as a tumor suppressor during the induction of disparate subtypes of AML in vivo. (a) Schema of the in vivo experiments. Ezh2fl/fl; WT or Ezh2fl/fl; Mx1-Cre+ mice were treated with pIpC to induce Ezh2 deletion in Mx1-Cre–expressing mice before retroviral transduction with either MLL-AF9 or AML1-ETO9a retrovirus followed by transplantation into lethally irradiated WT C57/Bl6 recipient mice. (b) Kaplan–Meier graph demonstrating significantly increased survival for Ezh2+/+; MLL-AF9 (WT) primary leukemias (n = 8 animals) vs. Ezh2−/−; MLL-AF9 primary leukemias (n = 8 animals, log-rank [Mantel–Cox] test P = 0.0341). (c) Kaplan–Meier graph demonstrating significantly increased survival for Ezh2+/+; AML1-ETO9a (WT) primary leukemias (n = 6 animals) vs. Ezh2−/−; AML1-ETO9a primary leukemias (n = 8 animals, log-rank [Mantel–Cox] test P = 0.0004). (d) Histopathology of spleen (left) and BM (right) taken at necropsy in Ezh2+/+ vs. Ezh2−/− AML1-ETO9a murine primary leukemias. Both samples show obvious and similar degrees of leukemic infiltration with large primitive blast cells that demonstrated a myeloid phenotype on flow cytometry, with no macroscopic or microscopic phenotypic difference demonstrated between the leukemias of either genotype (bars, 100 µm). *, P < 0.05; ***, P < 0.001.