A computational approach to the relationship between radiation induced double strand breaks and translocations.

W R Holley, A Chatterjee
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引用次数: 3

Abstract

A theoretical framework is presented which provides a quantitative analysis of radiation induced translocations between the ab1 oncogene on CH9q34 and a breakpoint cluster region, bcr, on CH 22q11. Such translocations are associated frequently with chronic myelogenous leukemia. The theory is based on the assumption that incorrect or unfaithful rejoining of initial double strand breaks produced concurrently within the 200 kbp intron region upstream of the second abl exon, and the 16.5 kbp region between bcr exon 2 and exon 6 interact with each other, resulting in a fusion gene. for an x-ray dose of 100 Gy, there is good agreement between the theoretical estimate and the one available experimental result. The theory has been extended to provide dose response curves for these types of translocations. These curves are quadratic at low doses and become linear at high doses.

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辐射诱导双链断裂与易位关系的计算方法。
提出了一个理论框架,提供了一个定量分析辐射诱导的易位之间的ab1致癌基因在CH9q34和断点簇区域,bcr,在ch22q11。这种易位常与慢性骨髓性白血病有关。该理论基于这样的假设:在第二个abl外显子上游200 kbp的内含子区域内同时产生的不正确或不忠实的初始双链断裂重新连接,以及bcr外显子2和外显子6之间16.5 kbp的区域相互作用,导致融合基因。对于100戈瑞的x射线剂量,理论估计和现有的一个实验结果吻合得很好。该理论已得到扩展,为这类易位提供了剂量反应曲线。这些曲线在低剂量时是二次曲线,在高剂量时变为线性曲线。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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