For two decades, leukaemia stem cells (LSCs) in chronic myeloid leukaemia (CML) and acute myeloid leukaemia (AML) have been advanced paradigms for the cancer stem cell field. In CML, the acquisition of the fusion tyrosine kinase BCR-ABL1 in a haematopoietic stem cell drives its transformation to become a LSC. In AML, LSCs can arise from multiple cell types through the activity of a number of oncogenic drivers and pre-leukaemic events, adding further layers of context and genetic and cellular heterogeneity to AML LSCs not observed in most cases of CML. Furthermore, LSCs from both AML and CML can be refractory to standard-of-care therapies and persist in patients, diversify clonally and serve as reservoirs to drive relapse, recurrence or progression to more aggressive forms. Despite these complexities, LSCs in both diseases share biological features, making them distinct from other CML or AML progenitor cells and from normal haematopoietic stem cells. These features may represent Achilles' heels against which novel therapies can be developed. Here, we review many of the similarities and differences that exist between LSCs in CML and AML and examine the therapeutic strategies that could be used to eradicate them.

中文翻译：

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白血病干细胞：CML 和 AML 的相似点、差异和临床前景。

二十年来，慢性粒细胞白血病（CML）和急性粒细胞白血病（AML）中的白血病干细胞（LSC）一直是癌症干细胞领域的先进范例。在 CML 中，造血干细胞中融合酪氨酸激酶 BCR-ABL1 的获得驱动其转变为 LSC。在 AML 中，LSC 可以通过多种致癌驱动因素和白血病前期事件的活动而由多种细胞类型产生，从而为 AML LSC 增加更多层次的背景以及遗传和细胞异质性，而在大多数 CML 病例中未观察到。此外，来自 AML 和 CML 的 LSC 可能对标准治疗无效，并且在患者体内持续存在，克隆多样化，并作为储存库，导致复发、再发或进展为更具侵袭性的形式。尽管存在这些复杂性，但这两种疾病中的 LSC 具有共同的生物学特征，使它们与其他 CML 或 AML 祖细胞以及正常造血干细胞不同。这些特征可能代表了新疗法的致命弱点。在这里，我们回顾了 CML 和 AML 中 LSC 之间存在的许多相似点和差异，并研究了可用于根除它们的治疗策略。