Subscribe to the gold package and get unlimited access to Shamra Academy
Register a new userRicci Flow and Entropy Model for Avascular Tumor Growth and Decay Control
131
0
0.0
(
0
)
Authors
Tijana T. Ivancevic
Ask ChatGPT about the research
No Arabic abstract
Prediction and control of cancer invasion is a vital problem in medical science. This paper proposes a modern geometric Ricci-flow and entropy based model for control of avascular multicellular tumor spheroid growth and decay. As a tumor growth/decay control tool, a monoclonal antibody therapy is proposed. Keywords: avascular tumor growth and decay, multicellular tumor spheroid, Ricci flow and entropy, nonlinear heat equation, monoclonal antibody cancer therapy
rate research
Read More
We propose a strange-attractor model of tumor growth and metastasis. It is a 4-dimensional spatio-temporal cancer model with strong nonlinear couplings. Even the same type of tumor is different in every patient both in size and appearance, as well as in temporal behavior. This is clearly a characteristic of dynamical systems sensitive to initial conditions. The new chaotic model of tumor growth and decay is biologically motivated. It has been developed as a live Mathematica demonstration, see Wolfram Demonstrator site: http://demonstrations.wolfram.com/ChaoticAttractorInTumorGrowth/ Key words: Reaction-diffusion tumor growth model, chaotic attractor, sensitive dependence on initial tumor characteristics
The comprehension of tumor growth is a intriguing subject for scientists. New researches has been constantly required to better understand the complexity of this phenomenon. In this paper, we pursue a physical description that account for some experimental facts involving avascular tumor growth. We have proposed an explanation of some phenomenological (macroscopic) aspects of tumor, as the spatial form and the way it growths, from a individual-level (microscopic) formulation. The model proposed here is based on a simple principle: competitive interaction between the cells dependent on their mutual distances. As a result, we reproduce many empirical evidences observed in real tumors, as exponential growth in their early stages followed by a power law growth. The model also reproduces the fractal space distribution of tumor cells and the universal behavior presented in animals and tumor growth, conform reported by West, Guiot {it et. al.}cite{West2001,Guiot2003}. The results suggest that the universal similarity between tumor and animal growth comes from the fact that both are described by the same growth equation - the Bertalanffy-Richards model - even they does not necessarily share the same biophysical properties.
Tumor growth has long been a target of investigation within the context of mathematical and computer modelling. The objective of this study is to propose and analyze a two-dimensional probabilistic cellular automata model to describe avascular solid tumor growth, taking into account both the competition between cancer cells and normal cells for nutrients and/or space and a time-dependent proliferation of cancer cells. Gompertzian growth, characteristic of some tumors, is described and some of the features of the time-spatial pattern of solid tumors, such as compact morphology with irregular borders, are captured. The parameter space is studied in order to analyze the occurrence of necrosis and the response to therapy. Our findings suggest that transitions exist between necrotic and non-necrotic phases (no-therapy cases), and between the states of cure and non-cure (therapy cases). To analyze cure, the control and order parameters are, respectively, the highest probability of cancer cell proliferation and the probability of the therapeutic effect on cancer cells. With respect to patterns, it is possible to observe the inner necrotic core and the effect of the therapy destroying the tumor from its outer borders inwards.
In this work, we study the in-vitro dynamics of the most malignant form of the primary brain tumor: Glioblastoma Multiforme. Typically, the growing tumor consists of the inner dense proliferating zone and the outer less dense invasive region. Experiments with different types of cells show qualitatively different behavior. Wild-type cells invade a spherically symmetric manner, but mutant cells are organized in tenuous branches. We formulate a model for this sort of growth using two coupled reaction-diffusion equations for the cell and nutrient concentrations. When the ratio of the nutrient and cell diffusion coefficients exceeds some critical value, the plane propagating front becomes unstable with respect to transversal perturbations. The instability threshold and the full phase-plane diagram in the parameter space are determined. The results are in a good agreement with experimental findings for the two types of cells.
We study a simplified stochastic model for the vascularization of a growing tumor, incorporating the formation of new blood vessels at the tumor periphery as well as their regression in the tumor center. The resulting morphology of the tumor vasculature differs drastically from the original one. We demonstrate that the probabilistic vessel collapse has to be correlated with the blood shear force in order to yield percolating network structures. The resulting tumor vasculature displays fractal properties. Fractal dimension, microvascular density (MVD), blood flow and shear force has been computed for a wide range of parameters.
Log in to be able to interact and post comments
comments
Fetching comments
Sign in to be able to follow your search criteria
