Understanding of the crosstalk between normal residual hematopoietic stem cells and the leukemic niche in acute myeloid leukemia

Abstract

Acute myeloid leukemia (AML) is a heterogenous disease, yet clinically most patients present with pancytopenia resulting from bone marrow (BM) failure, predisposing them to life-threatening infections and bleeding. The mechanisms by which AML mediate hematopoietic suppression is not well known. Indeed, much effort has so far focussed on how AML remodels the bone marrow niche to make it a more permissive environment, with less focus on how the remodelled niche impacts normal hematopoietic cells. In this perspective, we present evidence of the key role of the bone marrow niche in suppressing HSCs during leukemic progression and provide perspectives on how future research in this topic may be exploited to provide treatments for one of the key complications of AML.