Down for the count in acute myeloid leukemia

Abstract

In this issue of Blood, Rauch et al provide evidence for a novel mechanism to explain a fundamental yet enigmatic observation that has plagued hematologists for decades: the decline in nonleukemic hematopoiesis in the bone marrow of patients with acute myeloid leukemia (AML). The authors found that high expression of the thrombopoietin (TPO) receptor MPL on AML blasts predicts neutropenia and thrombocytopenia, and that AML blasts expressing high levels of MPL deplete TPO in cell culture and in mouse models. Rather than crowding out normal bone marrow hematopoietic stem cells (HSCs), might MPL-expressing AML blasts impair hematopoiesis by stealing the cytokine TPO?1