Chemotaxis effects on the vascular tumor growth: Phase-field model and simulations

In this paper, we propose a vascular tumor growth model that combines a phase-field tumor model with a phasefield angiogenesis model. By incorporating various tumor cell species, we capture the instabilities of the tumor in the presence of evolving neovasculature. The model not only considers different dynamics of tumor cell phase conversions, movement, and pressure effects but also provides a comprehensive representation of angiogenesis, encompassing chemotaxis of endothelial cells, sprouting, anastomoses, and blood flow in capillaries. This study evaluates the impact of chemotaxis on tumor cell movement in both avascular and vascular tumor growth scenarios. The results highlight the acceleration of tumor growth when angiogenesis is stimulated. Additionally, the investigation explores various initial distances of the tumor from neighboring vessels, revealing a critical threshold distance beyond which the angiogenesis factor fails to stimulate angiogenesis, resulting in the tumor maintaining a stable state. The integration of chemotaxis into the growth model induces instabilities, leading to increased nutrient availability and faster growth for the tumor. Furthermore, the study considers antiangiogenesis therapy as an ideal approach, assuming complete inhibition of angiogenesis from the early stages. In this scenario, the tumor persists in a steady state, adhering to the avascular size limit in the absence of neovasculature. Conversely, when considering chemotaxis, anti-angiogenesis therapy loses efficiency, enabling unrestrained tumor growth towards neighboring vessels. This work sheds light on the intricate interplay among chemotaxis, angiogenesis, and anti-angiogenesis therapy in the context of vascular tumor growth, providing valuable insights for the development of targeted treatment strategies.