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SDE-driven modeling of phenotypically heterogeneous tumors: The influence of cancer cell stemness
(2018)
We deduce cell population models describing the evolution of a tumor (possibly interacting with its
environment of healthy cells) with the aid of differential equations. Thereby, different subpopulations
of cancer cells allow accounting for the tumor heterogeneity. In our settings these include cancer
stem cells known to be less sensitive to treatment and differentiated cancer cells having a higher
sensitivity towards chemo- and radiotherapy. Our approach relies on stochastic differential equations
in order to account for randomness in the system, arising e.g., by the therapy-induced decreasing
number of clonogens, which renders a pure deterministic model arguable. The equations are deduced
relying on transition probabilities characterizing innovations of the two cancer cell subpopulations,
and similarly extended to also account for the evolution of normal tissue. Several therapy approaches
are introduced and compared by way of tumor control probability (TCP) and uncomplicated tumor
control probability (UTCP). A PDE approach allows to assess the evolution of tumor and normal
tissue with respect to time and to cell population densities which can vary continuously in a given set
of states. Analytical approximations of solutions to the obtained PDE system are provided as well.
A nonlocal stochastic model for intra- and extracellular proton dynamics in a tumor is proposed.
The intracellular dynamics is governed by an SDE coupled to a reaction-diffusion
equation for the extracellular proton concentration on the macroscale. In a more general context
the existence and uniqueness of solutions for local and nonlocal
SDE-PDE systems are established allowing, in particular, to analyze the proton dynamics model both,
in its local version and the case with nonlocal path dependence.
Numerical simulations are performed
to illustrate the behavior of solutions, providing some insights into the effects of randomness on tumor acidity.
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 propose a multiscale model for tumor cell migration in a tissue network. The system of equations involves a structured population model for the tumor cell density, which besides time and
position depends on a further variable characterizing the cellular state with respect to the amount
of receptors bound to soluble and insoluble ligands. Moreover, this equation features pH-taxis and
adhesion, along with an integral term describing proliferation conditioned by receptor binding. The
interaction of tumor cells with their surroundings calls for two more equations for the evolution of
tissue fibers and acidity (expressed via concentration of extracellular protons), respectively. The
resulting ODE-PDE system is highly nonlinear. We prove the global existence of a solution and
perform numerical simulations to illustrate its behavior, paying particular attention to the influence
of the supplementary structure and of the adhesion.
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.
In this paper we propose a phenomenological model for the formation of an interstitial gap between the tumor and the stroma. The gap
is mainly filled with acid produced by the progressing edge of the tumor front. Our setting extends existing models for acid-induced tumor invasion models to incorporate
several features of local invasion like formation of gaps, spikes, buds, islands, and cavities. These behaviors are obtained mainly due to the random dynamics at the intracellular
level, the go-or-grow-or-recede dynamics on the population scale, together with the nonlinear coupling between the microscopic (intracellular) and macroscopic (population)
levels. The wellposedness of the model is proved using the semigroup technique and 1D and 2D numerical simulations are performed to illustrate model predictions and draw
conclusions based on the observed behavior.
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.
The aim is to prove global existence and uniqueness of square integrable solutions to a class of multiscale models for tumour
cell migration involving chemotaxis, haptotaxis, and subcellular dynamics. This approach allows the tissue
fibre and cell densities as well as concentrations of chemotactic signals to be less regular and the conditions sufficient for well-posedness of the multiscale model to be less restrictive than in previous settings.
We propose and analyze a multiscale model for acid-mediated tumor invasion
accounting for stochastic effects on the subcellular level.
The setting involves a PDE of reaction-diffusion-taxis type describing the evolution of the tumor cell density,
the movement being directed towards pH gradients in the local microenvironment,
which is coupled to a PDE-SDE system characterizing the
dynamics of extracellular and intracellular proton concentrations, respectively.
The global well-posedness of the model is shown and
numerical simulations are performed in order to illustrate the solution behavior.
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.