Dissecting the molecular mechanism of chronic myelogenous leukemia using murine models.
Dissecting the molecular mechanism of chronic myelogenous leukemia using murine models.
复制标题
使用小鼠模型剖析慢性粒细胞白血病的分子机制。
DOI：
10.1080/1042819021000002875
复制
发表时间：
2002
影响因子：
2.6
通讯作者：
Ren,Ruibao
中科院分区：
文献类型：
--
作者：
Ren,Ruibao
慢性粒细胞白血病（CML）是一种复杂的疾病，其影响干细胞生物学、血液谱系确定和/或选择的调节以及造血细胞增殖、存活、粘附和迁移的总体调节。近年来，CML小鼠模型的建立使得能够在生物体水平上对CML发病机制的分子机制进行实验分析。本文综述了CML小鼠模型的建立方法，并分析了CML患者中由t（9;22）（q34;q11）易位产生的BCR-ABL癌蛋白的功能结构域和下游信号通路的作用，以及相关酪氨酸激酶癌蛋白、细胞因子产生改变和癌基因协同作用在CML样疾病发病机制中的作用。这些白血病发生的体内研究将有助于推进CML的治疗，以及了解白血病发生和造血的基本规则，这反过来又有助于开发其他相关疾病的治疗方法。
Chronic myelogenous leukemia (CML) is a complex disease that impinges on stem cell biology, the regulation of blood lineage determination and/or selection, as well as the overall regulation of hematopoietic cell proliferation, survival, adhesion and migration. Establishment of murine models for CML in recent years has enabled experimental analyses of molecular mechanisms in the pathogenesis of CML at the organismal level. This review summarizes the approaches used to develop murine models for CML and the analyses of the roles of functional domains and downstream signaling pathways of BCR-ABL (an oncoprotein generated by the t(9;22)(q34;q11) translocation found in CML patients) and the roles of related tyrosine kinase oncoproteins, altered cytokine production and oncogene cooperation in the pathogenesis of CML-like disease using murine models. These in vivo studies of leukemogenesis will help to advance therapies for CML, as well as to understand fundamental rules of leukemogenesis and hematopoiesis, which should contribute in turn to the development of therapies for other related diseases.