白血病及其骨髓微环境已知在疾病过程中会发生动态变化。然而，关于白血病细胞在循环中的动力学以及特定因素对循环中的白血病细胞（CLCs）清除的影响，目前所知甚少。为了对疾病进展和治疗反应期间的白血病细胞动态有一个基本的了解，我们在急性白血病的小鼠模型中应用了血液置换方法。我们发现，CLCs在血液中循环的时间比实体瘤细胞循环肿瘤细胞长1-2个数量级。我们进一步观察到：i）急性淋巴细胞白血病（ALL）模型中，骨髓中的白血病存在可以限制CLCs的清除，ii）复发性急性髓系白血病（AML）模型中，CLCs的清除速度比未经处理的对照组更快。我们的方法还可以直接量化微环境因素对CLCs清除性能的影响。例如，两个白血病模型的数据表明，血管粘附分子E-选择素可以改变CLCs的清除。我们的研究强调了CLCs的清除速率因肿瘤和治疗状态而异，并提供了一种识别调控循环细胞动力学的基本过程和因素的策略。

Leukemias and their bone marrow microenvironment are known to undergo dynamic changes over the course of disease. However, relatively little is known about the circulation kinetics of leukemia cells, nor the impact of specific factors on the clearance of circulating leukemia cells (CLCs) from the blood. To gain a basic understanding of leukemia cell dynamics over the course of disease progression and therapeutic response, we apply a blood exchange method to mouse models of acute leukemia. We find that CLCs circulate in the blood for 1-2 orders of magnitude longer than solid tumor circulating tumor cells. We further observe that: i) leukemia presence in the marrow can limit the clearance of CLCs in a model of acute lymphocytic leukemia (ALL), and ii) CLCs in a model of relapsed acute myeloid leukemia (AML) can clear faster than their untreated counterparts. Our approach can also directly quantify the impact of microenvironmental factors on CLC clearance properties. For example, data from two leukemia models suggest that E-selectin, a vascular adhesion molecule, alters CLC clearance. Our research highlights that clearance rates of CLCs can vary in response to tumor and treatment status and provides a strategy for identifying basic processes and factors that govern the kinetics of circulating cells.