Data from: Age-specific induction of mutant p53 drives clonal hematopoiesis and acute myeloid leukemia in adult mice

The investigation of the mechanisms behind p53 mutations in acute myeloid
leukemia (AML) has been limited by the lack of suitable mouse models,
which historically have resulted in lymphoma rather than leukemia. This
study introduces two new AML mouse models. One model induces mutant p53
and Mdm2 haploinsufficiency in early development, showing the role of Mdm2
in myeloid-biased hematopoiesis and AML predisposition, independent of
p53. The second model mimics clonal hematopoiesis by inducing mutant p53
in adult hematopoietic stem cells, demonstrating that the timing of p53
mutation determines AML versus lymphoma development. In this context,
age-related changes in hematopoietic stem cells (HSCs), collaborates with
mutant p53 to predispose towards myeloid transformation rather than
lymphoma development. Our study unveils new insights into the cooperative
impact of HSC age, Trp53 mutations and Mdm2 haploinsufficiency on clonal
hematopoiesis and the development of myeloid malignancies.