| Abstract: |
| Cancer invasion and metastasis are inherently multiscale processes driven by complex interactions between cancer cells and the tumour microenvironment. A central mechanism underlying cancer heterogeneity is the epithelial-to-mesenchymal transition (EMT), through which proliferative epithelial-like cancer cells (ECCs), forming the bulk of solid tumours, progressively acquire migratory and invasive mesenchymal-like traits. Mesenchymal-like cancer cells (MCCs) can actively invade surrounding tissue and disseminate to distant organs via the vasculature. At secondary sites, they may undergo the reverse mesenchymal-to-epithelial transition (MET), enabling metastatic growth. Importantly, EMT is a continuous process that gives rise to intermediate hybrid phenotypes with increasing invasive potential.
In this talk, we present a phenotype-dependent individual-based model together with its corresponding macroscopic formulation, incorporating continuous transitions along the epithelial-mesenchymal spectrum. This framework enables the study of the emergence and maintenance of phenotypic heterogeneity during tumour progression. Additionally, we investigate an individual-based model for MCC migration, focusing on the role of cell-cell adhesion in collective dynamics, informed by experimental data. In particular, we introduce a stochastic representation of N-cadherin-mediated adhesion, where bond lifetimes depend on the pulling force acting on the cells. |
|