In this work, we present a numerical study of the influence of matrix degrading enzyme (MDE) dynamics and haptotaxis on the development of vessel networks in tumor-induced angiogenesis. Avascular tumors produce growth factors that induce nearby blood vessels to emit sprouts formed by endothelial cells. These capillary sprouts advance toward the tumor by chemotaxis (gradients of growth factor) and haptotaxis (adhesion to the tissue matrix outside blood vessels). The motion of the capillaries in this constrained space is modelled by stochastic processes (Langevin equations, branching and merging of sprouts) coupled to continuum equations for concentrations of involved substances. There is a complementary deterministic description in terms of the density of actively moving tips of vessel sprouts. The latter forms a stable soliton-like wave whose motion is influenced by the different taxis mechanisms. We show the delaying effect of haptotaxis on the advance of the angiogenic vessel network by direct numerical simulations of the stochastic process and by a study of the soliton motion.
tumor-induced angiogenesis; haptotaxis; chemotaxis; soliton; collective coordinates; ensemble average