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The Fisher–Kolmogorov–Petrovsky–Piskunov model, also known as the Fisher–KPP model, supports travelling wave solutions that are successfully used to model numerous invasive phenomena with applications in biology, ecology and combustion theory. However, there are certain phenomena that the Fisher–KPP model cannot replicate, such as the extinction of invasive populations. The Fisher–Stefan model is an adaptation of the Fisher–KPP model to include a moving boundary whose evolution is governed by a Stefan condition. The Fisher–Stefan model also supports travelling wave solutions; however, a key additional feature of the Fisher–Stefan model is that it is able to simulate population extinction, giving rise to a spreading–extinction dichotomy . In this work, we revisit travelling wave solutions of the Fisher–KPP model and show that these results provide new insight into travelling wave solutions of the Fisher–Stefan model and the spreading–extinction dichotomy. Using a combination of phase plane analysis, perturbation analysis and linearization, we establish a concrete relationship between travelling wave solutions of the Fisher–Stefan model and often-neglected travelling wave solutions of the Fisher–KPP model. Furthermore, we give closed-form approximate expressions for the shape of the travelling wave solutions of the Fisher–Stefan model in the limit of slow travelling wave speeds, c ≪1.

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Continuum mathematical models for collective cell motion normally involve reaction-diffusion equations, such as the Fisher-KPP equation, with a linear diffusion term to describe cell motility and a logistic term to describe cell proliferation. While the Fisher-KPP equation and its generalisations are commonplace, a significant drawback for this family of models is that they are not able to capture the moving fronts that arise in cell invasion applications such as wound healing and tumour growth. An alternative, less common, approach is to include nonlinear degenerate diffusion in the models, such as in the Porous-Fisher equation, since solutions to the corresponding equations have compact support and therefore explicitly allow for moving fronts. We consider here a hole-closing problem for the Porous-Fisher equation whereby there is initially a simply connected region (the hole) with a nonzero population outside of the hole and a zero population inside. We outline how self-similar solutions (of the second kind) describe both circular and non-circular fronts in the hole-closing limit. Further, we present new experimental and theoretical evidence to support the use of nonlinear degenerate diffusion in models for collective cell motion. Our methodology involves setting up a two-dimensional wound healing assay that has the geometry of a hole-closing problem, with cells initially seeded outside of a hole that closes as cells migrate and proliferate. For a particular class of fibroblast cells, the aspect ratio of an initially rectangular wound increases in time, so the wound becomes longer and thinner as it closes; our theoretical analysis shows that this behaviour is consistent with nonlinear degenerate diffusion but is not able to be captured with commonly used linear diffusion. This work is important because it provides a clear test for degenerate diffusion over linear diffusion in cell lines, whereas standard one-dimensional experiments are unfortunately not capable of distinguishing between the two approaches.

Two-dimensional collective cell migration assays are used to study cancer and tissue repair. These assays involve combined cell migration and cell proliferation processes, both of which are modulated by cell-to-cell crowding. Previous discrete models of collective cell migration assays involve a nearest-neighbour proliferation mechanism where crowding effects are incorporated by aborting potential proliferation events if the randomly chosen target site is occupied. There are two limitations of this traditional approach: (i) it seems unreasonable to abort a potential proliferation event based on the occupancy of a single, randomly chosen target site; and, (ii) the continuum limit description of this mechanism leads to the standard logistic growth function, but some experimental evidence suggests that cells do not always proliferate logistically. Motivated by these observations, we introduce a generalised proliferation mechanism which allows non-nearest neighbour proliferation events to take place over a template of [Formula: see text] concentric rings of lattice sites. Further, the decision to abort potential proliferation events is made using a crowding function, f(C), which accounts for the density of agents within a group of sites rather than dealing with the occupancy of a single randomly chosen site. Analysing the continuum limit description of the stochastic model shows that the standard logistic source term, [Formula: see text], where λ is the proliferation rate, is generalised to a universal growth function, [Formula: see text]. Comparing the solution of the continuum description with averaged simulation data indicates that the continuum model performs well for many choices of f(C) and r. For nonlinear f(C), the quality of the continuum-discrete match increases with r.