Various models of tumour growth are available in the literature. The first type describe the evolution of the cell number density when considered as a continuous visco-elastic material with growth. The second type describe the tumour as a set, and rules for the free boundary are given related to the classical Hele-Shaw model of fluid dynamics. Following previous papers where the material is described by a purely elastic material, or when active cell motion is included, we make the link between the two types of description considering the 'stiff pressure law' limit. Even though viscosity is a regularizing effect, new mathematical difficulties arise in the visco-elastic case because estimates on the pressure field are weaker and do not immediately imply compactness. For instance, travelling wave solutions and numerical simulations show that the pressure is discontinuous in space, which is not the case for an elastic material.

Abstract. The hydrodynamic limit for a kinetic model of chemotaxis is investigated. The limit equation is a non local conservation law, for which finite time blow-up occurs, giving rise to measure-valued solutions and discontinuous velocities. An adaptation of the notion of duality solutions, introduced for linear equations with discontinuous coefficients, leads to an existence result. Uniqueness is obtained through a precise definition of the nonlinear flux as well as the complete dynamics of aggregates, i.e. combinations of Dirac masses. Finally a particle method is used to build an adapted numerical scheme. Mathematics

Existence and uniqueness of global in time measure solution for the multidimensional aggregation equation is analyzed. Such a system can be written as a continuity equation with a velocity field computed through a self-consistent interaction potential. In Carrillo et al. (Duke Math J (2011)) [16], a well-posedness theory based on the geometric approach of gradient flows in measure metric spaces has been developed for mildly singular potentials at the origin under the basic assumption of being λ-convex. We propose here an alternative method using classical tools from PDEs. We show the existence of a characteristic flow based on Filippov's theory of discontinuous dynamical systems such that the weak measure solution is the pushforward measure with this flow. Uniqueness is obtained thanks to a contraction argument in transport distances using the λ-convexity of the potential. Moreover, we show the equivalence of this solution with the gradient flow solution. Finally, we show the convergence of a numerical scheme for general measure solutions in this framework allowing for the simulation of solutions for initial smooth densities after their first blow-up time in L p -norms.

We formulate a Hele-Shaw type free boundary problem for a tumor growing under the combined effects of pressure forces, cell multiplication and active motion, the latter being the novelty of the present paper. This new ingredient is considered here as a standard diffusion process. The free boundary model is derived from a description at the cell level using the asymptotic of a stiff pressure limit.Compared to the case when active motion is neglected, the pressure satisfies the same complementarity Hele-Shaw type formula. However, the cell density is smoother (Lipschitz continuous), while there is a deep change in the free boundary velocity, which is no longer given by the gradient of the pressure, because some kind of 'mushy region' prepares the tumor invasion.

Kinetic-transport equations are, by now, standard models to describe the dynamics of populations of bacteria moving by run-and-tumble. Experimental observations show that bacteria increase their run duration when encountering an increasing gradient of chemotactic molecules. This led to a first class of models which heuristically include tumbling frequencies depending on the path-wise gradient of chemotactic signal.More recently, the biochemical pathways regulating the flagellar motors were uncovered. This knowledge gave rise to a second class of kinetic-transport equations, that takes into account an intra-cellular molecular content and which relates the tumbling frequency to this information. It turns out that the tumbling frequency depends on the chemotactic signal, and not on its gradient.For these two classes of models, macroscopic equations of Keller-Segel type, have been derived using diffusion or hyperbolic rescaling. We complete this program by showing how the first class of equations can be derived from the second class with molecular content after appropriate rescaling. The main difficulty is to explain why the path-wise gradient of chemotactic signal can arise in this asymptotic process.Randomness of receptor methylation events can be included, and our approach can be used to compute the tumbling frequency in presence of such a noise.

Mathematical models have been widely used to describe the collective movement of bacteria by chemotaxis. In particular, bacterial concentration waves traveling in a narrow channel have been experimentally observed and can be precisely described thanks to a mathematical model at the macroscopic scale. Such model was derived in [1] using a kinetic model based on an accurate description of the mesoscopic run-and-tumble process. We extend this approach to study the behavior of the interaction between two populations of E. Coli. Separately, each population travels with its own speed in the channel. When put together, a synchronization of the speed of the traveling pulses can be observed. We show that this synchronization depends on the fraction of the fast population. Our approach is based on mathematical analysis of a macroscopic model of partial differential equations. Numerical simulations in comparison with experimental observations show qualitative agreement.

We focus in this work on the numerical discretization of the one dimensional aggregation equation ∂ t ρ + ∂ x (vρ) = 0, v = a(W * ρ), in the attractive case. Finite time blow up of smooth initial data occurs for potential W having a Lipschitz singularity at the origin. A numerical discretization is proposed for which the convergence towards duality solutions of the aggregation equation is proved. It relies on a careful choice of the discretized macroscopic velocity v in order to give a sense to the product vρ. Moreover, using the same idea, we propose an asymptotic preserving scheme for a kinetic system in hyperbolic scaling converging towards the aggregation equation in hydrodynamical limit. Finally numerical simulations are provided to illustrate the results.

Several mathematical models of tumor growth are now commonly used to explain medical observations and predict cancer evolution based on images. These models incorporate mechanical laws for tissue compression combined with rules for nutrients availability which can differ depending on the situation under consideration, in vivo or in vitro. Numerical solutions exhibit, as expected from medical observations, a proliferative rim and a necrotic core. However, their precise profiles are rather complex, both in one and two dimensions.We study a simple free boundary model formed of a Hele-Shaw equation for the cell number density coupled to a diffusion equation for a nutrient. We can prove that a traveling wave solution exists with a healthy region separated from the progressing tumor by a sharp front (the free boundary) while the transition to the necrotic core is smoother. Remarkable is the pressure distribution which vanishes at the boundary of the proliferative rim with a vanishing derivative at the transition point to the necrotic core.