Cancer invasion and metastasis are inherently multiscale processes driven by complex interactions between cancer cells and the tumour microenvironment [1]. A central mechanism driving cancer heterogeneity is the Epithelial-to-Mesenchymal Transition (EMT), a cellular programming process through which predominantly proliferative epithelial-like cancer cells (ECCs), forming the main bulk of solid tumours, progressively acquire migratory and invasive mesenchymal-like traits. Mesenchymal-like cancer cells (MCCs) are capable of actively invading surrounding tissue through the extracellular matrix and may disseminate to distant organs via the vasculature. Upon arrival at secondary sites, they can undergo the reverse Mesenchymal-to-Epithelial Transition (MET), enabling the initiation of metastatic growth. Importantly, EMT should be considered as a continuous process rather than a binary switch, giving rise to intermediate hybrid phenotypes, where ECCs progressively lose certain behavioural characteristics and adopt new capabilities that make them more aggressive and eventually becoming fully MCCs [2]. This invasion–metastasis cascade works across different scales, with large populations of ECCs (approx. 10^9 cells) coexisting with smaller populations of MCCs (approx. 10^3). As a consequence, classical modelling approaches that rely solely on either atomistic or macroscopic descriptions fail to adequately capture the full dynamics of tumour progression. Individual-based models are analytically intractable and computationally prohibitive at the scale of large tumour growth, while continuum macroscopic models often struggle to capture the dynamic behaviour of small populations of highly migratory cells [3]. In this talk, I will present a novel 3D hybrid multiscale mathematical model [4], that couples individual-based representations of migrating cancer cells with continuum descriptions of tumour growth, illustrating how EMT-driven phenotypic changes influence macroscopic invasion patterns within a multi-organ framework. Finally, I will introduce a phenotype-structured population model that incorporates continuous transitions along the epithelial–mesenchymal spectrum, providing a tractable framework for studying the emergence and maintenance of phenotypic heterogeneity in cancer.