白血病干细胞的新认识

S. Qiu, Ming Wang, Jianxiang Wang
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引用次数: 1

摘要

人类急性髓性白血病(AML)起源于罕见的白血病干细胞(LSCs)。疾病的复发在一定程度上可归因于LSCs。目前,已经鉴定出许多AML LSCs的表面标记物,包括CD123、CD44、CLL-1、CD96、CD47、CD32、CD25和TIM-3。此外,针对某些标记物的单克隆抗体已在异种移植模型中证明有效。在我们最近的工作中,我们发现在相同剂量下,N-cadherin和Tie2阳性CD34 + CD38 - CD123 +群体在NOD/SCID小鼠中比阴性群体更有效地发生急性髓系白血病。同时,白血病小鼠骨髓的母细胞是可移植的。据推测,FLT3-ITD突变可能使LSCs在环境中具有更强的扩展能力。这些数据表明n -钙粘蛋白和Tie2作为LSC标志物在白血病的发展过程中非常重要。
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New insight of leukemic stem cell
Human acute myeloid leukemia (AML) derives from rare leukemic stem cells (LSCs). Relapse of disease can be ascribed to LSCs to some degree. Currently, a number of surface markers of AML LSCs have been identified, including CD123, CD44, CLL-1, CD96, CD47, CD32, CD25 and TIM-3. Moreover, monoclonal antibodies targeting some markers have demonstrated efficacy in xenotransplantation models. In our recent work, we found that N-cadherin and Tie2 positive CD34 + CD38 - CD123 + populations could develop acute myeloid leukemia more effectively in NOD/SCID mice than their negative counterparts at the same doses. Meanwhile, the blast cells from the bone marrow of leukemic mice are transplantable. It is speculated that FLT3-ITD mutation could make the LSCs more capable of expanding in the environment. These data suggested that N-cadherin and Tie2 were very important in development of leukemia as LSC markers.
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