Computational Oncology of Chemotaxis-Driven Tumour–Immune Spatial Patterning and Stability

Vollständiger Abstract

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We develop a reaction–diffusion–chemotaxis model for spatial tumour–immune–chemokine dynamics that couples logistic tumour growth, immune-mediated killing, chemokine-dependent immune recruitment, chemotactic migration, and signal production. For the non-dimensional system, we establish local classical solvability, nonnegativity, a uniform tumour-density bound, and global mass estimates for the immune and chemokine components. The tumour-free equilibrium is stable precisely when the baseline immune-control index satisfies σ0/δ>1, whereas positive homogeneous coexistence is characterized by a scalar nonlinear equation. Linearization in the Neumann Laplacian eigenbasis yields a mode-dependent cubic dispersion relation, showing that chemotaxis does not alter the tumour-invasion threshold but can destabilize homogeneous coexistence through a finite-wavelength oscillatory instability above a critical sensitivity ξc. A conservative finite-volume discretization with upwind chemotactic fluxes and implicit backward differentiation formula time integration is used to test these predictions. Numerical experiments recover the analytical equilibria and growth rates, identify the dominant unstable mode, reproduce the transition to spatial heterogeneity, and quantify the effects of immune recruitment, decay, and diffusion on the stability boundary. Grid-refinement, mass-balance, residual, and nonnegativity diagnostics support the computational reliability of the results.