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VEGFRVascular Endothelial Growth Factor Receptor
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The mice were divided into four groups: normal control group ( n = 44), diabetic group ( n = 44), diabetic + SA group (diabetic mice treated with SA injection n = 44), and diabetic + SA + vascular endothelial growth factor receptor (VEGFR)1-BL group (diabetic mice treated with SA injection and VEGFR 1 blocking antibody n = 24).
Erythrocytosis due to VEGFR TKIs was first reported by Alexandrescu et al in 2008.
In particular, the agent simultaneously inhibits VEGFR, FGFR and also RET which are especially involved in tumor angiogenesis and proliferation of thyroid cancer.
There are 3 known VEGF receptor tyrosine kinases, VEGFRs 1, 2, and 3, that are exclusively expressed in endothelial cells, hematopoietic stem cells, and tumor cells (14), (15).
The prognosis of metastatic breast cancer is worse in patients who overexpress HER2 and VEGFR [3], at least without targeted therapy.
Similarly, by inhibiting the tyrosine kinase domains of VEGFR-1, VEGFR-2, and VEGFR-3 and other receptors (Raf, PDGFR-B, KIT, FLT-3, and RET), the oral drug Nexavar (Bayer) may compare favourably to antibodies targeting VEGF / VEGFR signalling.
It also inhibits various oncogenic and tumor microenvironment kinases including VEGFR 1-3, KIT, RET, PDGFR, and FGFR, which individually and collectively impact upon tumor growth, formation of a stromal microenvironment and disease progression.
In cancer indications, VEGFR tyrosine kinase inhibitors have characteristically demonstrated benefit in a variety of cancers, though it has been well documented that the dosage and use of this class in combination with other therapies has been limited by side effects.
sup][3],[4] Famitinib is a novel multi-targeting TKI against VEGFR, platelet-derived growth factor receptor, stem cell factor receptor (c-KIT) and FMS-like tyrosine kinase-3 receptor developed in China, which has found to be effective for clear cell renal cell carcinoma in the preliminary clinical trial.
Lenvatinib exhibits rapid and potent inhibition of kinase activity1, simultaneously inhibiting the activity of VEGFR, FGFR and also RET which are especially involved in tumor angiogenesis and proliferation of thyroid cancer, and has been confirmed to possess a novel binding mode (Type V)1.
Wogonin had no effect on VEGFR 3 expression in HLECs, but at 10-100[micro]M, inhibited the VEGF-C (250 ng/ml)-induced phosphorylation of VEGFR-3 (Fig.