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A mathematical model of P53 gene regulatory networks under radiotherapy

机译:放射治疗下P53基因调控网络的数学模型

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摘要

P53, a vital anticancer gene, controls the transcription and translation of a series of genes, and implement the cell cycle arrest and cell apoptosis by regulating their complicated signal pathways. Under radiotherapy, cell can trigger internal self-defense mechanisms in fighting against genome stresses induced by acute ion radiation (IR). To simulate the investigating of cellular responding acute IR at single cell level further, we propose a model of P53 gene regulatory networks under radiotherapy. Our model can successfully implement the kinetics of double strand breaks (DSBs) generating and their repair, ataxia telangiectasia mutated (ATM) activation, as well as P53-MDM2 feedback regulating. By comparing simulations under different IR dose, we can try to find the optimal strategy in controlling of IR dose and therapy time, and provide some theoretical analysis to obtain much better outcome of radiotherapy further.
机译:P53是一种重要的抗癌基因,它控制一系列基因的转录和翻译,并通过调节其复杂的信号通路来实现细胞周期停滞和细胞凋亡。在放射疗法下,细胞可以触发内部自卫机制,以对抗由急性离子辐射(IR)引起的基因组压力。为了进一步模拟在单个细胞水平上对细胞反应性急性IR的研究,我们提出了放射治疗下的P53基因调控网络模型。我们的模型可以成功地实现双链断裂(DSB)生成及其修复,共济失调毛细血管扩张突变(ATM)激活以及P53-MDM2反馈调节的动力学。通过比较不同IR剂量下的模拟,我们可以尝试找到控制IR剂量和治疗时间的最佳策略,并提供一些理论分析以进一步获得更好的放射治疗效果。

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