PPM1D modulates hematopoietic cell fitness and response to DNA damage and is a therapeutic target in myeloid malignancy.

In the vehicle control, there was a nonsignificant trend in the peripheral blood toward Ppm1d T476∗-fl/+ cells having a competitive advantage and a significant difference observed in the HSC and multipotent progenitor pools ( Figure 3 B-C), consistent with human genetic data suggesting that PPM1D mutant blood cells expand more rapidly than TP53 mutant cells in an aging population. 27 , 28 In contrast, the Trp53 R172H-fl/+ cells outcompeted the Ppm1d T476∗-fl/+ cells after either cisplatin or radiation exposure, with significant differences observed in the radiation group ( Figure 3 D-G).

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