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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 consider the multiscale model for glioma growth introduced in a previous work and extend it to account
for therapy effects. Thereby, three treatment strategies involving surgical resection, radio-, and
chemotherapy are compared for their efficiency. The chemotherapy relies on inhibiting the binding
of cell surface receptors to the surrounding tissue, which impairs both migration and proliferation.
Certain brain tumours are very hard to treat with radiotherapy due to their irregular shape caused by the infiltrative nature of the tumour cells. To enhance the estimation of the tumour extent one may use a mathematical model. As the brain structure plays an important role for the cell migration, it has to be included in such a model. This is done via diffusion-MRI data. We set up a multiscale model class accounting among others for integrin-mediated movement of cancer cells in the brain tissue, and the integrin-mediated proliferation. Moreover, we model a novel chemotherapy in combination with standard radiotherapy.
Thereby, we start on the cellular scale in order to describe migration. Then we deduce mean-field equations on the mesoscopic (cell density) scale on which we also incorporate cell proliferation. To reduce the phase space of the mesoscopic equation, we use parabolic scaling and deduce an effective description in the form of a reaction-convection-diffusion equation on the macroscopic spatio-temporal scale. On this scale we perform three dimensional numerical simulations for the tumour cell density, thereby incorporating real diffusion tensor imaging data. To this aim, we present programmes for the data processing taking the raw medical data and processing it to the form to be included in the numerical simulation. Thanks to the reduction of the phase space, the numerical simulations are fast enough to enable application in clinical practice.
Glioma is a common type of primary brain tumor, with a strongly invasive potential, often exhibiting nonuniform, highly irregular growth. This makes it difficult to assess
the degree of extent of the tumor, hence bringing about a supplementary challenge for the treatment. It is therefore necessary to understand the
migratory behavior of glioma in greater detail.
In this paper we propose a multiscale model for glioma growth and migration. Our model couples the microscale dynamics (reduced to the binding of surface receptors to the
surrounding tissue) with a kinetic transport equation for the cell density on the mesoscopic level of individual cells. On the latter scale we also include the
proliferation of tumor cells via effects of interaction with the tissue. An adequate parabolic scaling yields a convection-diffusion-reaction equation, for which the coefficients
can be explicitly determined from the information about the tissue obtained by diffusion tensor imaging. Numerical simulations relying on DTI measurements confirm the biological
findings that glioma spreads
along white matter tracts.