Pancreatic cancer relies on opposing signalling pathways to drive its cellular diversity

Tumour progression and spread are influenced by a variety of factors. These include communication between cells, the presence of differing types of cellular lineage in a cancer (tumour heterogeneity) and variations in cellular states (a phenomenon called plasticity, which describes the adaptability of these cells). Plasticity is often coupled to a process called the epithelial–mesenchymal transition (EMT), which is associated with one type of cell (an epithelial cell) losing its usual characteristics and switching to resemble a different type of cell (a mesenchymal cell). All of the above contribute to a poor prognosis^1,2. Writing in Nature, Li et al.³ present evidence as to how communication between epithelial and mesenchymal cancer cells promotes tumour heterogeneity and cellular plasticity to drive malignant pancreatic cancer.