Aggressive acute myeloid leukemia in PU.1/p53 double-mutant mice

Abstract

PU.1 downregulation within hematopoietic stem and progenitor cells (HSPCs) is the primary mechanism for the development of acute myeloid leukemia (AML) in mice with homozygous deletion of the upstream regulatory element (URE) of PU.1 gene. p53 is a well-known tumor suppressor that is often mutated in human hematologic malignancies including AML and adds to their aggressiveness; however, its genetic deletion does not cause AML in mouse.

Keywords

• Aggressive acute myeloid leukemia
• PU.1/p53
• differentiation
• microRNA
• p53
• AML