Analysis of virotherapy in solid tumor invasion
Stability of solutions to ordinary differential equations (34D20) Traveling wave solutions (35C07) Reaction-diffusion equations (35K57) PDEs in connection with biology, chemistry and other natural sciences (35Q92) Finite difference methods for initial value and initial-boundary value problems involving PDEs (65M06) Cell movement (chemotaxis, etc.) (92C17) Medical applications (general) (92C50)
In this paper, two mathematical models for the dynamics of tumour growth in the presence of oncolytic viruses and immune system cells (cytotoxic T-cells) are developed and analysed. First, the authors present a spatially homogeneous system of ordinary differential equations: \[ \dot x=\sigma-x+\frac{\gamma_1 x z}{\eta_1+z}-\nu xz\quad\text{(cytotoxic T-cells)}, \] \[ \dot y=\alpha_1 y(1-\alpha_2 y)-\frac{\theta_1 zy}{\eta_2+z}\quad\text{(uninfected tumour cells)}, \] \[ \dot z=\beta_1 z(1-\beta_2 z)+\frac{\theta_2 z y}{\eta_2+z}-\mu xz\quad\text{(infected tumour cells)}. \] A linear stability analysis of stationary states is made; in a nutshell, tumour-free steady states are unstable, whereas -- at least in a specific, biologically sensible parameter situation -- a steady state reflecting tumour dormancy is asymptotically stable. Numerical simulations are given. The ODE model is extended to a spatially heterogeneous framework including diffusion of tumour and immune system cells as well as chemotaxis of the latter towards increasing concentrations of a specific signalling substance. It is assumed that cytotoxic T-cells are supplied only in a specific spatial subdomain to invade the cancerous tissue afterwards. The dynamics of the resulting reaction-diffusion system in one spatial dimension are numerically simulated using finite differences. In a simplified setting (e.g. neglecting chemotactic effects), travelling wave solutions are derived analytically.
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