Figure 3.
HSCs with dominant negative mutations in Trp53 outcompete those with Ppm1d truncating mutations after radiation. (A) Schematic of competition experiment between Trp53R172H/+;Vav-Cre+;Cd45.1/2 and Ppm1dT476∗-fl/+;Vav-Cre+;Cd45.2 bone marrow cells transplanted into lethally irradiated Cd45.1 recipients. Cisplatin was dosed intraperitoneally at 4 mg/kg and sublethal irradiation was dosed at 2.5 Gy. (B-C) Peripheral blood CD11b+ (B) or bone marrow (C) CD45.2 chimerism in vehicle treated recipient mice. (D-E) Peripheral blood CD11b+ (D) or bone marrow (E) CD45.2 chimerism in cisplatin treated recipient mice. (F-G) Peripheral blood CD11b+ (F) or bone marrow (G) CD45.2 chimerism in radiation (XRT) treated recipient mice. Error bars show SEM, ∗P < .01, ∗∗P < .0001, ns, not significant.

HSCs with dominant negative mutations in Trp53 outcompete those with Ppm1d truncating mutations after radiation. (A) Schematic of competition experiment between Trp53R172H/+;Vav-Cre+;Cd45.1/2 and Ppm1dT476-fl/+;Vav-Cre+;Cd45.2 bone marrow cells transplanted into lethally irradiated Cd45.1 recipients. Cisplatin was dosed intraperitoneally at 4 mg/kg and sublethal irradiation was dosed at 2.5 Gy. (B-C) Peripheral blood CD11b+ (B) or bone marrow (C) CD45.2 chimerism in vehicle treated recipient mice. (D-E) Peripheral blood CD11b+ (D) or bone marrow (E) CD45.2 chimerism in cisplatin treated recipient mice. (F-G) Peripheral blood CD11b+ (F) or bone marrow (G) CD45.2 chimerism in radiation (XRT) treated recipient mice. Error bars show SEM, ∗P < .01, ∗∗P < .0001, ns, not significant.

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