Resumen
Anti-angiogenic therapies targeting the vascular endothelial growth factor (VEGF) signaling are established in the arsenal of cancer treatments. Despite the expectations, their benefits are temporary in cancer patients, partly due to the compensatory function of other angiogenic growth factors. This review focuses on the role of basic fibroblast growth factor (bFGF), one of the highly implicated players in the emergence of resistance to anti-angiogenic approaches. Here, we summarize data from various tumor types where bFGF is upregulated after anti-angiogenic treatment, the molecular mechanisms involved, and we highlight the current status and future perspectives of multi-target anti-angiogenic drugs for cancer.