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. 2019 May 10;104(11):2215–2224. doi: 10.3324/haematol.2018.205351

Figure 1.

Figure 1.

Aml1-ETO ameliorates the key features of the myeloproliferative neoplasm phenotype caused by K-RasG12D. (A) Schematic representation of in vivo competitive transplant experiment. (B-I) Analysis of recipients of Mx1-Cretg/+ controls; CON (n=13), Aml1ETO/+;Mx1-Cretg/+; AM (n=14), KrasG12D/+;Mx1-Cretg/+; KM (n=12) and Aml1ETO/+;KrasG12D/+;Mx1-Cretg/+; AKM fetal liver (FL) (n=14) for (B) peripheral blood (PB) white blood cell (WBC) count. (C) PB hemoglobin levels. (D) Bone marrow (BM) cellularity per tibia and femur. (E and F) CD45.2 Mac1+Gr1lo myeloid cells as absolute number in the PB (E) and spleen (F). (G) Representative FACS plots of Mac1+Gr1+ and Mac1+Gr1lo myeloid cells as a percentage of LiveCD19CD4CD8aNK1.1CD45.2+ cells across all experiments in the PB. (H) Spleen weight. (I) Platelet count. Results were generated in three independent experiments. The results were analyzed using multiple comparison ANOVA and are presented as mean±Standard Deviation. *P<0.05; **P<0.01; ***P<0.001; ****P<0.0001.