Moleculaire afwijkingen en doelgerichte therapieën in blaaskanker

Bladder cancer is characterized by a high mutational burden and a wide spectrum of molecular alterations, underscoring their central role in tumorigenesis and therapeutic decision-making. Recent advances have identified clinically relevant alterations in the fibroblast growth factor receptor 3 (FGFR3), trophoblast cell surface antigen 2 (Trop-2), nectin cell adhesion molecule 4 (Nectin-4), and programmed death-ligand 1 (PD-L1). These molecular changes have led to the development of targeted therapies, such as FGFR inhibitors, antibody-drug conjugates, and immune checkpoint inhibitors, which have already demonstrated significant clinical benefit in selected patient groups. However, the heterogeneity of bladder cancer highlights the limitations of single biomarkers in predicting therapeutic response and prognosis. Future directions emphasize biomarker-driven and integrative approaches, combining multiple molecular biomarkers, molecular subtypes, and molecular analyses to refine patient selection and expand therapeutic opportunities. Such strategies hold potential to further personalize treatment and improve clinical outcomes for patients with bladder cancer.