Fusion genes in leukemia: an emerging network
Fusion genes in leukemia: an emerging network
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DOI：
10.1159/000056818
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发表时间：
2000-01-01
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影响因子：
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通讯作者：
Bohlander, SK
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文献类型：
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作者：
Bohlander, SK
对反复发生的染色体重排，特别是易位和倒位的分子分析，为我们深入了解血液恶性肿瘤的发病机制提供了有价值的信息。许多易位导致位于易位断裂点的基因融合。近年来，我们目睹了白血病染色体易位数量的迅速上升，其特征在于在分子水平上。然而.新鉴定为易位融合基因的基因数量没有以同样的速度增加。这是由于多个基因参与了一个以上的易位，与许多其他伴侣基因形成融合基因。人们不仅发现了星形拓扑结构，其中一个基因与其他几个基因（例如ETV 6/PDGFRB，ETV 6/JAK 2，ETV 6/ABL等）融合，而且还包括将几个基因与多于一个融合配偶体连接的网络（例如ETV 6/RUNX 1（AML 1）、RUNX 1/CBFA 2 T1（ETO）、ETV 6/EVI 1、RUNX 1/EVI 1、ETV 6/ABL、BCR/ABL）。这种网络的出现，以及基因在新的融合组合中的“再循环”，表明可以改变导致白血病的基因数量相当有限。版权所有（C）2001 S. Karger AG，巴塞尔。
The molecular analysis of recurring chromosome rearrangements, especially of translocations and inversions, has provided us with valuable insight into the pathogenesis of hematological malignancies. Many translocations result in the fusion of genes located at the translocation breakpoints. In recent years we have witnessed a rapid rise in the number of chromosome translocations in leukemias being characterized at the molecular level. However. the number of genes being newly identified as translocation fusion genes has not risen at the same pace. This is due to the fact that several genes are involved in more than one translocation forming fusion genes with a number of other partner genes. Not only does one find star-shaped topologies, with one gene farming fusions with several others (e.g. ETV6/PDGFRB, ETV6/JAK2, ETV6/ABL etc.), but also networks connecting several genes with more than one fusion partner (e.g. ETV6/RUNX1 (AML1), RUNX1/CBFA2T1 (ETO), ETV6/EVI1, RUNX1/EVI1, ETV6/ABL, BCR/ABL). The emergence of such networks with the ''recycling" of genes in new fusion combinations suggests that there is a rather limited number of genes which can be altered to cause leukemia. Copyright (C) 2001 S. Karger AG, Basel.