摘要
完全根除慢性粒细胞白血病在这个高度选择性和强效BCR-ABL络氨酸激酶抑制剂(TKIs)的时代仍具有挑战性。基于TKI治疗CML的难题是TKI不能有效的靶向CML干细胞。已经有几个通路诱导TKI在静态CML干细胞中的不敏感性。本文描述了BCR-ABL/HAUSP/PTEN基因网络,这些信号传导介质能够调节肿瘤抑制基因PTEN的功能。为研究CML干细胞根除,我们也标明了PTEN功能的病理学方法。
关键词: 人第10号染色体缺失的磷酸酶及张力蛋白同源基因,体内外能对p53去泛素的蛋白,BCR-ABL激酶基因,慢性髓细胞样白血病
Current Drug Targets
Title:Unleashing the Guardian: The Targetable BCR-ABL/HAUSP/PML/PTEN Network in Chronic Myeloid Leukemia
Volume: 18 Issue: 4
关键词: 人第10号染色体缺失的磷酸酶及张力蛋白同源基因,体内外能对p53去泛素的蛋白,BCR-ABL激酶基因,慢性髓细胞样白血病
摘要: The complete eradication of Chronic Myeloid Leukemia is still challenging even in the era of highly selective and potent BCR-ABL tyrosine kinase inhibitors (TKIs). The ‘Achilles heel’ of TKI-based CML therapy is the inability of TKI to effectively target CML stem cells. Several pathways have been described to induce TKI insensitiveness in quiescent CML stem cells. In this review, we will describe the BCR-ABL/HAUSP/PML/PTEN network, whose signaling mediators converge to regulate the function of the tumor suppressor PTEN. We will also highlight the pharmacological strategies to modulate PTEN functions in order to sustain CML stem cell eradication.
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Cite this article as:
Unleashing the Guardian: The Targetable BCR-ABL/HAUSP/PML/PTEN Network in Chronic Myeloid Leukemia, Current Drug Targets 2017; 18 (4) . https://dx.doi.org/10.2174/1389450117666160608120527
DOI https://dx.doi.org/10.2174/1389450117666160608120527 |
Print ISSN 1389-4501 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5592 |
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