Lack of expression of Thy-1 (CD90) on acute myeloid leukemia cells with long-term proliferative ability in vitro and in vivo
Lack of expression of Thy-1 (CD90) on acute myeloid leukemia cells with long-term proliferative ability in vitro and in vivo
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DOI：
10.1182/blood.v89.9.3104
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发表时间：
1997-05-01
期刊：
影响因子：
20.3
通讯作者：
Sutherland, HJ
中科院分区：
文献类型：
--
作者：
Blair, A;Hogge, DE;Sutherland, HJ
急性髓系白血病(AML)被认为是由一小部分白血病前体细胞维持的，为了确定这类细胞在体内外具有长期增殖能力的表型，我们采用悬浮培养2~8周后白血病克隆性细胞(CFU)的产生作为体外衡量这些细胞的指标，并将它们的表型与能够移植到非肥胖型糖尿病严重联合免疫缺陷(NOD/SCID)小鼠的细胞进行比较。检测白血病原始细胞CD34和Thy-1(CD90)抗原的表达。大多数确诊的AML原始细胞缺乏Thy-1的表达。大多数原代CFU-BLAST和悬浮培养至8周的CFU均为CD34(+)/Thy-1(-)。然而，来自一名AML M5患者的CD34(+)/Thy-1(-)和CD34(-)亚组分都实现了显著的植入。这些结果表明，尽管个体之间存在异质性，但在体内和体外能够维持疾病Bn的白血病祖细胞不同于正常的造血祖细胞，因为它们缺乏Thy-1的表达。(C)1997年由美国血液病学会主办。
Acute myeloid leukaemia (AML) is thought to be maintained by a small population of leukemic progenitor cells, To define the phenotype of such cells with long-term proliferative capacity in vitro and in vivo, we have used the production of leukemic clonogenic cells (CFU) after 2 to 8 weeks in suspension culture as a measure of these cells in vitro and compared their phenotype with that of cells capable of engrafting nonobese diabetic severe combined immune deficient (NOD/SCID) mice. Leukemic blast peripheral blood cells were evaluated for expression of CD34 and Thy-1 (CD90) antigens. The majority of AML blast cells at diagnosis lacked expression of Thy-1. Most primary CFU-blast and the CFU detected at up to 8 weeks from suspension cultures were CD34(+)/Thy-1(-).:AML cells that were capable of engrafting NOD/SCID mice were also found to have the CD34(+)/ Thy-1(-) phenotype. However, significant engraftment was achieved using both CD34(+)/Thy-1(-) and CD34(-) subfractions from one AML M5 patient. These results suggest that while heterogeneity exists between individual patients, the leukemic progenitor cells that are capable of maintaining the disease Bn vitro and in vivo differ from normal hematopoietic progenitor cells in their lack of expression of Thy-1. (C) 1997 by The American Society of Hematology.