In this paper, we consider the following PDE-ODE system modelling cancer invasion with slow diffusion and ECM remodelling,

\[ \begin{cases} u_t=\Delta u^m-\chi\nabla\cdot(u\nabla v)-\xi\nabla\cdot(u\nabla\omega)+\mu u(1-u-\omega), \\ v_t=\Delta v+u-v, \\ \omega_t={-}v\omega+\eta \omega(1-u-\omega). \end{cases} \]

$\eta =0$

$\eta >0$

$\eta =0$

$\eta >0$

This paper considers a model for oncolytic virotherapy given by the doubly haptotactic cross-diffusion system

\[ \left\{\begin{array}{@{}ll} u_t=D_u\Delta u-\xi_u\nabla\cdot(u\nabla v)+\mu_u u(1-u)-\rho uz,\\ v_t={-} (\alpha_u u+\alpha_w w)v,\\ w_t=D_w\Delta w-\xi_w\nabla\cdot(w\nabla v)- w+\rho uz,\\ z_t=D_z\Delta z-\delta_z z- \rho uz+\beta w, \end{array}\right. \]

$D_u,D_w,D_z,\xi _u,\xi _w,\delta _z,\rho$

$\alpha _u,\alpha _w,\mu _u,\beta$

$\Omega \subset {\mathbb {R}}^{2}$

$\beta <1$

$(u,v,w,z)$

$(1, 0, 0, 0)$

$(L^{\infty }(\Omega ))^{4}$

$t\rightarrow \infty$

This study considers a model for oncolytic virotherapy, as given by the reaction–diffusion–taxis system

\[\begin{eqnarray*} \left\{ \begin{array}{l} u_t = \Delta u - \nabla (u\nabla v)-\rho uz, \\ v_t = - (u+w)v, \\ w_t = D_w \Delta w - w + uz, \\ z_t = D_z \Delta z - z - uz + \beta w, \end{array} \right. \end{eqnarray*}\]

Previous analysis has asserted that for all reasonably regular initial data, an associated no-flux type initial-boundary value problem admits a global classical solution, and that this solution is bounded if β < 1, whereas whenever β > 1 and $({1}/{|\Omega |})\int _\Omega u(\cdot ,0) > 1/(\beta -1)$, infinite-time blow-up occurs at least in the particular case when ρ = 0.

In order to provide an appropriate complement to this, the current study reveals that for any ρ ⩾ 0 and arbitrary β > 0, at each prescribed level γ ∈ (0, 1/(β − 1)+) one can identify an L∞-neighbourhood of the homogeneous distribution (u, v, w, z) ≡ (γ, 0, 0, 0) within which all initial data lead to globally bounded solutions that stabilize towards the constant equilibrium (u∞, 0, 0, 0) with some u∞ > 0.

We propose and study a class of parabolic-ordinary differential equation models involving chemotaxis and haptotaxis of a species following signals indirectly produced by another, non-motile one. The setting is motivated by cancer invasion mediated by interactions with the tumour microenvironment, but has much wider applicability, being able to comprise descriptions of biologically quite different problems. As a main mathematical feature constituting a core difference to both classical Keller–Segel chemotaxis systems and Chaplain–Lolas type chemotaxis–haptotaxis systems, the considered model accounts for certain types of indirect signal production mechanisms. The main results assert unique global classical solvability under suitably mild assumptions on the system parameter functions in associated spatially two-dimensional initial-boundary value problems. In particular, this rigorously confirms that at least in two-dimensional settings, the considered indirectness in signal production induces a significant blow-up suppressing tendency also in taxis systems substantially more general than some particular examples for which corresponding effects have recently been observed.

In a planar smoothly bounded domain $\Omega$ , we consider the model for oncolytic virotherapy given by

$$\left\{ \begin{array}{l} u_t = \Delta u - \nabla \cdot (u\nabla v) - uz, \\[1mm] v_t = - (u+w)v, \\[1mm] w_t = d_w \Delta w - w + uz, \\[1mm] z_t = d_z \Delta z - z - uz + \beta w, \end{array} \right.$$

$ D_w $

$ D_z $

$\beta$

$\beta \lt 1$

$M \gt 0$

$\beta \gt 0$

$$u\ge M \qquad \mbox{in } \Omega\times (0,\infty).$$

$\beta \gt 1$

$$\liminf_{t\to\infty} \inf_{x\in\Omega} u(x,t)\le \frac{1}{\beta-1}.$$

$\beta$

$\beta = 1$

A model of tumor growth in a spatial environment is analyzed. The model includesproliferating and quiescent compartments of tumor cells indexed by successively mutated cell phenotypesof increasingly proliferative aggressiveness. The model incorporates spatial dependencedue to both random motility and directed movement haptotaxis. The model structures tumor cellsby both cell age and cell size. The model consists of a system of nonlinear partial differentialequations for the compartments of tumor cells, extracellular matrix, matrix degradative enzyme,and oxygen. The existence, uniqueness, positivity, regularity, and growth characteristics of thesolutions are investigated.

This paper provides a detailed stochastic analysis of leucocyte cell movement based on the dynamics of a rigid body. The cell's behavior is studied in two relevant anisotropic environments displaying adhesion mediated movement (haptotaxis) and stimulus mediated movement (chemotaxis). This behavior is modeled by diffusion processes on three successively longer time scales, termed locomotion, translocation, and migration.