Speaker
Description
Cancer invasion and metastasis are multiscale processes driven by complex interactions between cancer cells and the tumour microenvironment. A key 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 generates intermediate hybrid phenotypes with progressively increasing invasive potential. In this talk, we will explore a variety of models that incorporate phenotypic transitions for cancer invasion across mathematical and biological scales. Firstly, I will introduce a novel 3D hybrid multiscale model which couples individual-based representations of migrating cancer cells with continuum descriptions of tumour growth. The model illustrates how EMT-driven phenotypic changes shape macroscopic invasion patterns within a multi-organ framework. Furthermore, I will present a phenotype-dependent individual based model and its corresponding macroscopic model, which incorporates continuous transitions along the epithelial–mesenchymal spectrum, providing a tractable framework to study the emergence and maintenance of phenotypic heterogeneity in cancer.
