Fig. 3: Hematopoietic stem/progenitor compartments in the BM of diseased mice. | Leukemia

Fig. 3: Hematopoietic stem/progenitor compartments in the BM of diseased mice.

From: A unique role of p53 haploinsufficiency or loss in the development of acute myeloid leukemia with FLT3-ITD mutation

Fig. 3

a Percentages and absolute cell number of Lin, LT-HSC, and CMP cells in the BM. Data of other hematopoietic stem/progenitor cells were presented in Supplementary Fig. 9. Reduction of LT-HSCs in FLT3-ITD/ITD and ITD/ITD; p53+/− mice is consistent with a recent published report demonstrating that FLT3-ITD knock-in impairs HSC quiescence/homeostasis, leading to the depletion of LT-HSC [43]. The data shown in graphs represent means ± SD. *p < 0.05, **p < 0.01, n.s. no significant difference. Lin: lineage negative cells; LT-HSC: long-term hematopoietic stem cells (Linc-Kit+Sca-1+CD48CD150+); CMP: common myeloid progenitors (LinIL-7Rαc-Kit+Sca-1CD34+FcgR). WT (wild-type): n = 3 mice; ITD/ITD: n = 6; p53+/−: n = 6; ITD/ITD; p53+/−: n = 6. b Representative flow cytometric analysis showing increased leukemic CMP in mouse #1376. CMP was increased 66-fold in #1376 compared with WT mice. Of note, the frequencies of LSK, CMP and GMP in WT mice were very similar to published data (e.g., 0.29% LSK in our studies vs. 0.24% reported by Sitnicka et al. [44] and CMP: 0.23% vs. 0.13% [44]).

Back to article page