Molecular mechanisms for stemness maintenance of acute myeloid leukemia stem cells

Abstract

Human acute myeloid leukemia (AML) is a fatal hematologic malignancy characterized with accumulation of myeloid blasts and differentiation arrest. The development of AML is associated with a serial of genetic and epigenetic alterations mainly occurred in hematopoietic stem and progenitor cells (HSPCs), which change HSPC state at the molecular and cellular levels and transform them into leukemia stem cells (LSCs). LSCs play critical roles in leukemia initiation, progression, and relapse, and need to be eradicated to achieve a cure in clinic. Key to successfully targeting LSCs is to fully understand the unique cellular and molecular mechanisms for maintaining their stemness. Here, we discuss LSCs in AML with a focus on identification of unique biological features of these stem cells to decipher the molecular mechanisms of LSC maintenance.