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We prove the global existence, along with some basic boundedness properties, of weak solutions to a PDE-ODE system modeling the multiscale invasion of tumor cells through the surrounding tissue matrix. The model has been proposed in [22] and accounts on the macroscopic level for the evolution of cell and tissue densities, along with the concentration of a chemoattractant, while on the subcellular level it involves the binding of integrins to soluble and insoluble components of the peritumoral region. The connection between the two scales is realized with the aid of a contractivity function characterizing the ability of the tumor cells to adapt their motility behavior
to their subcellular dynamics.
The resulting system, consisting of three partial and three ordinary differential equations including a temporal delay, in particular involves chemotactic and haptotactic cross-diffusion. In order to overcome technical obstacles stemming from the corresponding highest-order interaction terms, we base our analysis on a certain functional, inter alia involving the cell and tissue densities in the diffusion and haptotaxis terms respectively, which is shown to enjoy a quasi-dissipative property. This will be used as a starting point for the derivation of a series of integral estimates finally allowing for the construction of a generalized solution as the limit of solutions to suitably regularized problems.
We propose and study a strongly coupled PDE-ODE system with tissue-dependent degenerate diffusion and haptotaxis that can serve as a model prototype for cancer cell invasion through the
extracellular matrix. We prove the global existence of weak solutions and illustrate the model behaviour by numerical simulations for a two-dimensional setting.
We propose and study a strongly coupled PDE-ODE-ODE system modeling cancer cell invasion through a tissue network
under the go-or-grow hypothesis asserting that cancer cells can either move or proliferate. Hence our setting features
two interacting cell populations with their mutual transitions and involves tissue-dependent degenerate diffusion and
haptotaxis for the moving subpopulation. The proliferating cells and the tissue evolution are characterized by way of ODEs
for the respective densities. We prove the global existence of weak solutions and illustrate the model behaviour by
numerical simulations in a two-dimensional setting.
We investigate a PDE-ODE system describing cancer cell invasion in a tissue network. The model is an extension of the multiscale setting in [28,40], by considering two subpopulations of tumor cells interacting mutually and with the surrounding tissue. According to the go-or-grow hypothesis, these subpopulations consist of moving and proliferating cells, respectively. The mathematical setting also accommodates the effects of some therapy approaches. We prove the global existence of weak solutions to this model and perform numerical simulations to illustrate its behavior for different therapy strategies.
We study a multi-scale model for growth of malignant gliomas in the human brain.
Interactions of individual glioma cells with their environment determine the gross tumor shape.
We connect models on different time and length scales to derive a practical description of tumor growth that takes these microscopic interactions into account.
From a simple subcellular model for haptotactic interactions of glioma cells with the white matter we derive a microscopic particle system, which leads to a meso-scale model for the distribution of particles, and finally to a macroscopic description of the cell density.
The main body of this work is dedicated to the development and study of numerical methods adequate for the meso-scale transport model and its transition to the macroscopic limit.