Abstract

Acute myeloid leukemia (AML) is a hematologic malignancy, arising within the bone marrow, which is characterized by the uncontrolled proliferation of leukemic blasts, often in association with a disruption of normal hematopoiesis. Like their normal counterparts, AML cells depend upon both cell-intrinsic and -extrinsic regulatory signals generated by their surrounding microenvironment, for their survival and proliferation. AML has long been considered a hematopoietic-cell autonomous disorder in which disease initiation and progression is driven by hematopoietic cell intrinsic genetic events.

Recent experimental findings in diverse model systems have challenged this view, implicating different stromal cells of the bone marrow in disease pathogenesis. Thus it is now accepted that leukemic hematopoiesis can turn the BM niche into a “leukemic niche” which promotes leukemic stem cell (LSC) function and impairs the maintenance of normal HSC. However, much remains to be understood about how different leukemic cells impacts the BM microenvironment and, in turn, how changes in the activity of specific BM niche cells contribute to AML pathogenesis. This talk will highlight some of the current understanding of the alterations of BM niche components and how the dialogue between leukemic and stromal cells participated in leukemogenesis.