Biology of CML stem cells: the basis for clinical heterogeneity?

Leukemia supplements Pub Date : 2012-08-01 Epub Date: 2012-08-09 DOI:10.1038/leusup.2012.23
J M Goldman, M Gordon, A Bazeos, D Marin
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引用次数: 3

Abstract

Although chronic myeloid leukemia (CML) is now defined on the basis of the presence of the BCR-ABL1 fusion gene, which may or may not be the initial genetic event that triggers the inappropriate expansion of the myeloid cell mass, CML, similar to other leukemias, is in fact clinically heterogeneous. The biological basis for this heterogeneity is unknown. Here, we summarize some of the data illustrating this heterogeneity and speculate about possible mechanisms that may cause it. It could, for example, be intrinsic in the leukemia stem cell or could be related to some aspect of the patient's response to the leukemia.

CML干细胞生物学:临床异质性的基础?
尽管慢性髓性白血病(CML)现在的定义是基于BCR-ABL1融合基因的存在,这可能是也可能不是触发髓性细胞团不适当扩张的初始遗传事件,但CML与其他白血病相似,实际上在临床上是异质性的。这种异质性的生物学基础尚不清楚。在这里,我们总结了一些说明这种异质性的数据,并推测可能导致这种异质性的机制。例如,它可能是白血病干细胞固有的或者可能与病人对白血病反应的某些方面有关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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