Abstract
Helicobacter pylori (H. pylori) bacterium is widely studied risk factor of gastric cancer. The mechanism by which H. pylori induces gastric carcinogenesis, has been studied by various researcher. However, a molecular level mechanism by which H. pylori enters into the cells causes p53 modulation leads to stress and gastric cancer developments, is still an open question. In the present studied we developed p53-ROS-H. pylori model integrated deterministic model to show the molecular level interaction between p53 proteins network and H. pylori bacterium via reactive oxygen species. The interactions among p53 network proteins, reactive oxygen species and H. pylori are described by system of a set of ordinary differential equations. The rate of the reaction has been set by using pervious experimental and theoretical works. These sets of differential equations further numerically solved by using standard Runge-Kutta fourth order method at high computational cost. Numerical simulation results showed that as the accumulation of H. pylori (IcHP) in the cells increases, the instability of p53 network systems are also increase. Various phases of the system have been observed viz normal phase, stable to damp phase, damped to stable phase and stationary phase. These phases correspond to various stages of cell cycle. The present model clarifies the molecular level interactions between H. pylori via reactive oxygen species. This model suggests that as the accumulation of H. pylori reaches at a particular threshold value, it leads to the cancerous progression. The suggested model will be very useful to understand the temporal dynamics of gastric cancer progression due to H. pylori bacterium. Further, study is needed in realistic environment.