Abstract

Radiotherapy can induce DNA damage into cells and trigger the cell cycle arrest and cell apoptosis by regulating the vital genes and their signal pathways. To illustrate the cellular self-defense mechanisms in fighting against genome stresses under radiotherapy, a model of P53 stress response networks is proposed by using the methods with the system biology and cyber-biology at single cell level. The kinetics of Double Strand Breaks (DSBs) generation and repair, ARF and ATM activation, P53-MDM2 feedback regulation, as well as the toxins degradation are presented versus continuous radiation time. The model provides a theoretical framework to illustrate the complicated kinetics in cellular response to acute IR under radiotherapy.

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