Understanding cancer pathogenesis requires knowledge of not only the specific contributory genetic mutations, but also the cellular framework in which they arise and function. Here we explore the clonal evolution of a form of childhood precursor-B cell acute lymphoblastic leukemia that is characterized by a chromosomal translocation generating a TEL-AML1 fusion gene. We identify a cell compartment in leukemic children that can propagate leukemia when transplanted in mice. By studying a monochorionic twin pair,one preleukemic and one with frank leukermia, we establish the lineal relationship between these "cancer-propagating" cells and the preleukemic cell in which the TEL-AML1 fusion first arises or has functional impact. Analysis of TEL-AML1 transduced cord blood cells suggests that TEL-AML1 functions as a first-hit mutation by endowing this preleukemic cell with altered self-renewal and survival properties.
[Science,2008;(10).1126]
参考译文
理解癌症的发病机制不仅需要认识基因突变的特殊作用，还要了解细胞骨架和它们的功能。这里我们探讨了一种儿童前B细胞急性淋巴细胞性白血病的克隆演变。这种病的特征之一是发生了染色体易位，产生了 TEL-AML1 融合基因。我们在白血病儿童的细胞中找到一个细胞区域，把这种细胞移植到老鼠身上可以产生白血病。通过研究一对单绒毛膜双胞胎，一个是前白血病状态，一个是真正的白血病患者，我们确定了“癌症扩散”细胞和前白血病细胞存在线性相关。TEL-AML1 的融合首先出现在前白血病细胞或者会对其产生功能影响。TEL-AML1 转导的脐带血细胞分析表明TEL-AML1 的功能可以改变前白血病细胞的自我更新和生存特性，从而可以作为突变的第一击。
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