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首页> 外文期刊>Cell cycle >Chimeric IgH-TCRalpha/delta translocations in T lymphocytes mediated by RAG.
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Chimeric IgH-TCRalpha/delta translocations in T lymphocytes mediated by RAG.

机译：RAG介导的T淋巴细胞中的嵌合IgH-TCRalpha /δ易位。

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摘要

Translocations involving the T cell receptor alpha/delta (TCRalpha/delta) chain locus, which bring oncogenes in the proximity of the TCRalpha enhancer, are one of the hallmark features of human T cell malignancies from ataxia telangiectasia (AT) and non-AT patients. These lesions are frequently generated by the fusion of DNA breaks at the TCRalpha/delta locus to a disperse region centromeric of the immunoglobulin heavy chain (IgH) locus. Aberrant VDJ joining accounts for TCRalpha/delta associated DNA cleavage, but the molecular mechanism that leads to generation of the "oncogene partner" DNA break is unclear. Here we show that in ATM deficient primary mouse T cells, IgH/TCRalpha/delta fusions arise at a remarkably similar frequency as in human AT lymphocytes. Recombinase-activating gene (RAG) is responsible for both TCRalpha/delta as well as IgH associated breaks on chromosome 12 (Chr12), which are subject to varying degrees of chromosomal degradation. We suggest a new model for how oncogenic translocations can arise from two non-concerted physiological DSBs.
机译：涉及T细胞受体alpha /δ（TCRalpha / delta）链基因座的易位使癌基因接近TCRalpha增强子，是共济失调性毛细血管扩张症（AT）和非AT患者的人类T细胞恶性肿瘤的标志性特征之一。 。这些损伤通常是由TCRalpha /δ位点的DNA断裂与免疫球蛋白重链（IgH）位点的着丝粒分散区融合而产生的。异常的VDJ连接导致了TCRalpha /δ相关的DNA切割，但是导致“癌基因伴侣” DNA断裂的分子机制尚不清楚。在这里，我们显示在ATM缺陷型原代小鼠T细胞中，IgH / TCRalpha /δ融合体的出现频率与人AT淋巴细胞中的频率非常相似。重组酶激活基因（RAG）负责12号染色体（Chr12）上的TCRalpha /δ和IgH相关断裂，这些断裂易受不同程度的染色体降解。我们建议一个新的模型，以探讨如何从两个未经证实的生理DSB引起致癌易位。

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