They quickly progress to VEGF inhibitors. In the Phase III trial Bleomycin Blenoxane of sorafenib versus placebo TARGET, patients achieved with the h Chsten concentration of VEGF gr Ere relative advantage of the VEGFR-TKI sorafenib than those with lower concentrations. But other studies have also revealed how AVOREN, inconsistent results, perhaps because bevacizumab has been tested in combination. Other studies have shown that the expression of groups of molecular biological factors are h Frequently in cancer patients. For example, we recently found that the signature Including six angiogenic markers Lich OPN, VEGF, sCA9, collagen IV, sVEGFR 2 and tumor identified necrosis factor-related apoptosis-inducing ligand, the patients received a gr Eren benefit of sorafenib PFS only that of sorafenib plus IFN. We also analyzed Pr Predictors of Transport PFS benefit from different treatment pazopanib versus placebo in the Phase III trial and found that.
IL-6 is a pr Diktiv, with hazard ratios of 0.31 in the high IL-6 group and 0.55 lower in the group. Placebo patients with high IL-6 had a significantly shorter PFS than those with low distinguished not IL-6, IL-6, but groups significantly in the arm pazopanib. Such high concentration of IL-6 predicted the benefit of pazopanib versus placebo, suggesting that the negative prognostic effect of high IL-6 attenuated Was weakened by pazopanib. High concentrations of six angiogenic factors and immune modulators in this analysis, IL-6, IL-8, HGF, OPN, VEGF and TIMP 1 showed a negative effect on OS interesting significant advantage compared to an operating system of pazopanib. Taken together, these suggest vorl Ufigen results suggest that patients with metastatic kidney cancer gain g and a high expression of angiogenic factors Eren advantage over to VEGF targeted therapies. Relevance, we have identified recently featured two groups of cancer patients CCRCC by their expression of angiogenic factors or inflammatory circulating substitution. Biological activity of t L Slicher factors being studied as a biomarker of biological activity t of VEGF inhibitors. According to their mechanisms of action, increases hte VEGF and placental growth factor-2 and sVEGFR and sVEGFR by 3 w During treatment with VEGFR-TKI. Commonly, gr Ere Ver Changes in patients with response to treatment, but the intensity of t the modulation of these factors varies greatly between individuals, and h Depends on the particular drug, its power and profile of molecular targets inhibited this is for many medications available big.
Single nucleotide polymorphisms are genetic determinants of drug exposure in the h They usually analyzed germline DNA from peripheral blood. SNPs have an impact on drug selection, dosage and / or optimization of the planning and early intervention to the specific toxicity of t. In two recent studies have germline SNP variants in angiogenesis-related genes and associated exposure with the response and tolerance to pazopanib and sunitinib in patients with advanced renal cell carcinoma associated established. Resistance largely to the fa, A plurality of anti-cancer agents, such as chemotherapy k Can induce responses other than those that angiogenesis inhibitors of cell growth of several tumor target cytokines to induce chemokines, growth factors, k can Cur.