Key result
Treatment with VEGF signaling inhibitors for cancer often induces proteinuria and hypertension, which may make it difficult to continue treatment long-term.
Different VEGF signaling inhibitors induce distinct pathological renal lesions, such as glomerular microangiopathy and collapsing glomerulopathy, which may complicate long-term cancer treatment.
Cancer growth depends on an abundant supply of nutrients, oxygen and vessels. Vascular endothelial growth factors (VEGFs), especially VEGF-A, are important factors that support cancer neovascularization (1). Therefore, inhibition of VEGF signaling has been successfully used to treat various cancers (2, 3). Typical reagents used are inhibitory antibodies against VEGF-A (bevacizumab) or VEGF receptor 2 (VEGFR2, ramucirumab), soluble VEGFR1/VEGFR2 extracellular domains (aflibercept), or receptor tyrosine kinase inhibitors (RTKIs, such as sunitinib), which interfere with the signaling downstream of VEGFR2 (1). Treatment with such reagents often induces proteinuria and hypertension, which may make it difficult to continue treatment long-term (1-5).
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Kiyoshi Mori (2022) conducted a review in Cancer. VEGF signaling inhibitors was evaluated on Proteinuria and hypertension. Treatment with VEGF signaling inhibitors for cancer often induces proteinuria and hypertension, which may make it difficult to continue treatment long-term.
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