In the current study, the authors investigated the effect of vascular endothelial growth factor (VEGF)-targeted therapy in this distinct subtype of RCC.
We found two SNPs (VEGFArs2010963 and VEGFR3 rs448012) that were significantly associated with increased risk of ccRCC, after adjusting for multiple comparisons [rs2010963 CC/GC cf.
We reviewed the clinical efficacy of axitinib after nivolumab treatment failure in six patients with metastatic renal cell carcinoma (RCC); the patients had received nivolumab treatment following vascular endothelial growth factor receptor (VEGFR) inhibitors.
However, the results of studies investigating the association between VEGF polymorphisms and renal cell carcinoma risk are inconsistent.Thus, a meta-analysis was performed.
5-LO was frequently overexpressed in von Hippel-Lindau protein (pVHL)-reduced tumors and in Vascular Endothelial Growth Factor (VEGF)-positive tumors, which represent two frequent alterations in CC-RCC.
A prospective, longitudinal cohort study was conducted with 50 patients diagnosed with clear-cell renal cell carcinoma to analyze VHL mutations and hypermethylation as well as VHL, HIF1-α, vascular endothelial growth factor (VEGF), ERK1/2, and ERK5 protein expression.
And VEGF-rs699947 polymorphism was also identified an increased risk of renal cell carcinoma (RCC) in allelic, heterozygote, dominant, homozygote, and recessive models.
A middle-aged man with conventional clear cell renal cell carcinoma (RCC) had received multiple prior systemic treatments including vascular endothelial growth factor receptor tyrosine kinase inhibitors, as well as multiple surgeries and radiotherapy treatments.
The associations between five polymorphisms of VEGF (rs3025039, rs699947, rs10434, rs1570360, and rs2010963) and renal cell carcinoma (RCC) risk have been extensively investigated, but the currently available results are inconsistent and inconclusive.
There has been a recent expansion of therapeutic options in metastatic renal cell carcinoma (RCC) targeted at the vascular endothelial growth factor and mammalian target of rapamycin pathways, which are fundamental to the biology of RCC.
In summary, our study showed evidence that the VEGFrs699947 polymorphism was obviously associated with an increased risk of bladder cancer and renal cell carcinoma, particularly in Asian population, while no significant association was observed in overall urologic neoplasms.
We revealed that there are significant ethnic differences in the C702T and G1612A allele frequencies, but suggested that C702T, C936T and G1612A polymorphisms in the 3'-UTR of VEGF gene are not associated with the risk of RCC, at least in Japanese population.
In clear cell renal cell carcinoma (CCRCC), vascular endothelial growth factor (VEGF) represents the central positive mediator of tumour angiogenesis while VEGF receptor (VEGFR) is the primary target of anti-angiogenic therapies.
VHL loss drives tumor angiogenesis and accounts for the clinical activity of VEGF receptor (VEGFR) tyrosine kinase inhibitors (TKIs), the first-line standard of care for advanced RCC.