利用随机算法与常微分方程，本论文建立了含外部放射性辐射和抗癌药物的p53调控网络的确定性和随机性模型；该调控网络模型包含了PTEN/PIP3/AKT主导的正反馈循环、p53/Mdm2/AKT主导的负反馈循环、抗癌药物Nutlin对Mdm2的结合作用和放射性辐射对DNA损坏的作用。用matlab对该网络模型进行了计算随机模拟。模拟发现p53含量变化与Nutlin浓度的时间积分有关，且p53含量的增长与药物剂量的增长存在非线性关系，这反映了抗癌药物的累积效应。在摄入药物前，系统就存在高度不规则振荡，多个细胞的平均轨迹变化趋势与确定性轨迹十分相似，不同细胞的震荡轨迹有明显的差异，这种差异给细胞的调控机制带来了“随机稳健性”。当PTEN循环不能正常运转时,PTEN含量较低，使得激活的AKT含量保持较高水平，从而大部分Mdm2被磷酸化、进入细胞核，使p53含量降低；摄入药物Nutlin后，p53的含量并没有大幅度降低、仍保持在了较高水平，这说明对于缺少完整的PTEN正反馈而致癌的细胞，Nutlin能发挥抗癌作用。

Using stochastic algorithms and ordinary differential equations, we establishes a deterministic and stochastic model of regulation network of p53 containing external irradiation and antitumor drug. This regulation network contains PTEN/PIP3/AKT positive feedback loops, p53 /Mdm2/AKT negative feedback loop, the antitumor drug Nutlin that interferes with Mdm2 and irradiation-induced DNA damage. The simulation result of the network by Matlab show that the p53 amount is related to the time integral of Nutlin , and the p53 amount has a nonlinear relationship with the drug dose. The system exhibits highly irregular fluctuation before the Nutlin exposure. The average stochastic trajectory of multiple cells is similar to the deterministic trajectory, and the stochastic trajectories of different cells are significantly different, which lead to what might be called "stochastic robustness" in cell regulation. When the PTEN mediated loop is broken, the low level of PTEN and the high level of activated AKT lead to amount of Mdm2actived entering cell nucleus which results in the p53 level low. When exposing to the Nutlin, instead of the rapid degradation the p53 still remain at a relatively high level indicating that Nutlin is an effective antitumor drug for cancer cell that lacks of intact PTEN positive feedback.