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Three-dimensional finite element computations of a cancer invasion model with nonlinear density-dependent diffusion and haptotactic sensitivity function are presented. The nonlinear model includes three key variables, namely the cancer cell density, the extra cellular matrix (ECM) density and the matrix degrading enzymes (MDE) concentration. In order to investigate the effects of tumor growth and invasion on a realistic geometry, the interactions between the cancer cells and the host tissue are incorporated into the model. The convergence study and the validation are first performed for the proposed numerical scheme. Then the effects of nonlinear diffusion and ECM-dependent haptotaxis on tumor growth and invasion in three-dimensional geometries are presented. Finally, several numerical simulations are performed with different combinations of nonlinear diffusion and haptotaxis functions to get an insight into the tumor invasion on a realistic (breast) geometry. The proposed computational model can be used to predict the location and shape of the tumor in realistic geometries at a particular instance. [ABSTRACT FROM AUTHOR]

Cell adhesion is a fundamental mechanism binding a cell to a surface, extracellular matrix or another cell through cell adhesion molecules. This cell behavior is involved in various biological processes including embryogenesis, migration and invasion, wound healing and tissue remodeling. This paper investigates the existence of traveling wavefronts of a nonlocal reaction-diffusion model. We provide a valid approach by using perturbation methods and the Banach fixed point theorem to show the existence of wavefronts for the model with some suitable parameter values. Numerically, the solutions with initial step functions eventually stabilize to a smooth wavefront for a relatively small adhesion coefficient. We also consider the application of this model to study the cancer invasion process, which results in a system with solutions reflecting the relation between cell-cell and cell-matrix adhesion in the cancer invasion regulation. Using the same method employed in the cell-adhesion model, the existence of traveling wavefronts to this system is established. Finally numerical simulations are presented to verify the effectiveness of our proposed theoretical results and to demonstrate some new phenomena that deserve further study in the future. [ABSTRACT FROM AUTHOR]

Reports on the ability of green tea flavanoid to lower the invasive potential of prostate cancer, according to scientists in Italy. Investigation of the molecular mechanisms triggered by the main green tea flavanoid; Inhibition of tumor growth by green-tea regimen; Activation of tumor-released pro-matrix metalloproteinase 2 by co-incubation of transgenic adenocarcinoma of mouse prostate-C1 cells with polymorphonuclear phagocytes.

Presents a study on the capability of green tea flavonoid to lower the invasive potential of prostate cancer. Evaluation of the action of epigallocatechin-3-gallate; Suppression of the activation of pro-matrix metalloproteinase 2; Potential of preventing the inflammatory involvement of prostate carcinoma.

Reports on the study which shows that host-derived plasminogen activator inhibitor-1 (PAI-1) sustains tumoral angiogenesis. Role of PAI-1 in tumor progression; Inhibition of tumor vascularization; Implications of the study.