cancerinvasion

Cancer invasion refers to the process by which malignant cells spread from a primary tumor into adjacent normal tissues, breaching the surrounding basement membranes and infiltrating the stromal matrix. It is a local phenomenon that can precede metastasis, but invasion itself describes the initial, tissue-level infiltration rather than distant spread through blood or lymphatics.

Mechanisms of invasion involve multiple coordinated changes. Epithelial-to-mesenchymal transition (EMT) reduces cell–cell adhesion and increases motility. Cancer cells remodel the extracellular matrix through proteolytic enzymes such as matrix metalloproteinases, vascular and fibroblast-derived factors, and altered cell–matrix interactions. Cytoskeletal reorganization and altered signaling through pathways including TGF-β, Wnt, Rho GTPases, and PI3K/AKT support invasive behavior. Tumor microenvironment components—cancer-associated fibroblasts, immune cells, and the ECM—also contribute to invasion by creating tracks and releasing pro-invasive signals. Tumor cells may invade as cohesive groups, individual cells, or via structures such as perineural or vascular routes.

Clinical significance and detection: invasion is associated with higher tumor grade, more aggressive behavior, and poorer prognosis. Histopathology commonly reports invasion into adjacent tissues, perineural invasion, or lymphovascular invasion. Imaging and surgical assessment aim to define invasion to guide resection margins and staging.

Therapeutic implications and research: direct anti-invasion therapies have been challenging, with limited success in clinical practice. Strategies focus on blocking ECM degradation, EMT processes, and tumor-stroma interactions, as well as targeting mechanobiology. Research uses 3D culture systems and in vivo imaging to study invasion dynamics and identify potential therapeutic targets.