PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 34104226-2 2021 Moreover, the combination regimen of atezolizumab (anti-programmed cell death protein ligand 1 antibody) plus bevacizumab (anti-vascular endothelial growth factor monoclonal antibody) has recently been demonstrated to have superior efficacy when compared with sorafenib monotherapy. Sorafenib 260-269 vascular endothelial growth factor A Homo sapiens 128-162 34434234-0 2021 Efficacy of Sorafenib Combined with Interventional Therapy on Primary Liver Cancer Patients and Its Effect on Serum AFP, VEGF, and GGT. Sorafenib 12-21 vascular endothelial growth factor A Homo sapiens 121-125 34434234-1 2021 Objective: To explore the efficacy of sorafenib combined with interventional therapy on primary liver cancer (PLC) patients and its effect on serum AFP, VEGF, and GGT. Sorafenib 38-47 vascular endothelial growth factor A Homo sapiens 153-157 34838486-3 2022 Vascular Endothelial Growth Factor inhibitors have different mechanisms of action, targeting either the ligand (e.g. bevacizumab, anti-Vascular Endothelial Growth Factor monoclonal antibody; aflibercept, recombinant anti-Vascular Endothelial Growth Factor fusion protein), or its receptors such as tyrosine kinase inhibitors (e.g. sunitinib or sorafenib). Sorafenib 344-353 vascular endothelial growth factor A Homo sapiens 0-34 34089726-8 2021 AuNPs could deliver new sorafenib derivatives into tumor tissues, and downregulate the expression of VEGF and VEGFR-2, as well as suppress migration, EMT, and angiogenesis in vitro. Sorafenib 24-33 vascular endothelial growth factor A Homo sapiens 101-105 33948974-7 2021 Hormonal pharmaceuticals, including melatonin, exerts proapoptotic via regulating matrix metallopeptidase activity while nonhormonal pharmaceutical sorafenib exerts antiproliferative effect via MAPK/ERK pathway and antiangiogenesis activity via VEGF/VEGFR pathway. Sorafenib 148-157 vascular endothelial growth factor A Homo sapiens 245-249 35245519-0 2022 Antitumor effects of rhamnazinon sorafenib-treated human hepatocellular carcinoma cell lines via modulation of VEGF signaling and PI3K/NF-kappaB p38/caspase-3 axes cross talk. Sorafenib 33-42 vascular endothelial growth factor A Homo sapiens 111-115 35245519-1 2022 AIMS: Hepatocellular carcinoma (HCC) is the most common liver malignancy,characterized by dysregulation of multiple oncogenic signaling pathways, including the VEGF/PI3K/NF-kappaB and p38 MAPK axes.Sorafenib is a multikinase inhibitor that targets Raf kinases and receptor tyrosine kinases,which mediate HCC angiogenesis.Rhamnazin is a VEGFR2 signaling inhibitor, which inhibits the phosphorylation of Vascular endothelial growth factor receptor 2(VEGFR2) and its downstream signaling regulators. Sorafenib 198-207 vascular endothelial growth factor A Homo sapiens 160-164 35245519-9 2022 SIGNIFICANCE: Rhamnazin potentiates the chemotherapeutic effect of sorafenib via modulation ofthe VEGF/PI3K/NF-kappaBsignaling axis, downregulation of VEGFR2 expression, and upregulation of the p38MAPK/caspase-3 axis in human HCC cell lines. Sorafenib 67-76 vascular endothelial growth factor A Homo sapiens 98-102 35016637-2 2022 Sorafenib, which inhibits the VEGF pathway, has an immune-modulation function but lacks substantial clinical data. Sorafenib 0-9 vascular endothelial growth factor A Homo sapiens 30-34 35234063-9 2022 In the HepG2 xenografts model, sorafenib plus SDC exhibited greater suppression on tumor growth than individual treatment accompanied with decreased expression of VEGF, VEGFA, Ki67, CD31 and increased expression of caspase-3. Sorafenib 31-40 vascular endothelial growth factor A Homo sapiens 163-167 35234063-9 2022 In the HepG2 xenografts model, sorafenib plus SDC exhibited greater suppression on tumor growth than individual treatment accompanied with decreased expression of VEGF, VEGFA, Ki67, CD31 and increased expression of caspase-3. Sorafenib 31-40 vascular endothelial growth factor A Homo sapiens 169-174 33860837-2 2021 Sorafenib resistance may be related to Src-induced cell migration and angiogenesis, which are regulated by cancer stem cell activation and release of vascular endothelial growth factor. Sorafenib 0-9 vascular endothelial growth factor A Homo sapiens 150-184 33860837-14 2021 Sorafenib and dasatinib combined treatment suppresses cell migration and angiogenesis by inhibiting the Src/FAK phosphorylation, cell-to-cell contact, cancer stem cell activation, and release of vascular endothelial growth factor. Sorafenib 0-9 vascular endothelial growth factor A Homo sapiens 195-229 31471309-6 2019 RESULTS: VEGF and PlGF increased after 4 weeks on sunitinib or sorafenib (P < 0.0001 for both) and returned to baseline at 6 weeks on sunitinib (corresponding to the break in the sunitinib schedule) but not sorafenib (which was administered continuously). Sorafenib 63-72 vascular endothelial growth factor A Homo sapiens 9-13 33485105-5 2021 All compounds significantly inhibited VEGF stimulated migration of HUVECs at 10 microM dose with (3a, 3e, 3g, 3h and 3l) showing better or comparable inhibitory activities to that of sorafenib. Sorafenib 183-192 vascular endothelial growth factor A Homo sapiens 38-42 33080958-4 2020 While the activity of immunotherapy agents as single agents seems to be limited to an "ill-defined" small subset of patients, the combination of the anti PD-L1 atezolizumab and anti-vascular endothelial growth factor bevacizumab revealed a benefit in the outcomes when compared to sorafenib in the first line. Sorafenib 281-290 vascular endothelial growth factor A Homo sapiens 182-216 32521890-10 2020 CONCLUSION: Compared with TACE alone, Sorafenib combined with TACE can significantly improve ORR and DCR, obviously reduce the levels of serum VEGF, bFGF and AFP, and prolong the survival of patients with advanced hepatocellular carcinoma, while the adverse reactions are tolerable, so it is worthy of clinical popularization and application. Sorafenib 38-47 vascular endothelial growth factor A Homo sapiens 143-147 33640712-13 2021 CONCLUSIONS: The findings of this study demonstrate that the expression of HIF-2alpha, VEGFA and EphA2 can be inhibited by sorafenib, and that sorafenib is likely to provide an effective adjunct treatment for patients with HCC following HIFU ablation. Sorafenib 123-132 vascular endothelial growth factor A Homo sapiens 87-92 33402115-1 2021 BACKGROUND: Sequential inhibition of the vascular endothelial growth factor (VEGF) pathway with sorafenib could be useful for patients with metastatic renal cell carcinoma (RCC). Sorafenib 96-105 vascular endothelial growth factor A Homo sapiens 41-75 33402115-1 2021 BACKGROUND: Sequential inhibition of the vascular endothelial growth factor (VEGF) pathway with sorafenib could be useful for patients with metastatic renal cell carcinoma (RCC). Sorafenib 96-105 vascular endothelial growth factor A Homo sapiens 77-81 33195657-13 2020 CONCLUSION: Adaption from lenvatinib to sorafenib is a feasible method to improve the anti-VEGF therapy-induced nephrotic syndrome and achieve the therapeutic goal at the same time. Sorafenib 40-49 vascular endothelial growth factor A Homo sapiens 91-95 30722031-2 2019 The first VEGF inhibitors approved for mRCC were sorafenib and sunitinib. Sorafenib 49-58 vascular endothelial growth factor A Homo sapiens 10-14 31497714-5 2019 Interestingly, Sorafenib released from Pluronic silica NPs completely prevented endothelial cell responses and postreceptor mitogen-activated protein kinase signaling ignited by vascular endothelial growth factor, one of the major players of tumor angiogenesis. Sorafenib 15-24 vascular endothelial growth factor A Homo sapiens 178-212 31391334-9 2019 The immune modulation resulted from sorafenib-mediated blockade of signaling through the VEGF/VEGFR/flt-3 pathway, affecting ERK phosphorylation. Sorafenib 36-45 vascular endothelial growth factor A Homo sapiens 89-93 30543051-1 2019 The use of vascular endothelial growth factor inhibitors such as sorafenib is limited by a risk of severe cardiovascular toxicity. Sorafenib 65-74 vascular endothelial growth factor A Homo sapiens 11-45 31195212-2 2019 Sorafenib, regorafenib, lenvatinib and cabozantinib are tyrosine kinase inhibitors (TKIs) that target, in part, vascular endothelial growth factor receptors, and are approved in various regions of the world for the treatment of advanced HCC. Sorafenib 0-9 vascular endothelial growth factor A Homo sapiens 112-146 31646819-9 2019 CONCLUSIONS: Sorafenib combined with Avastin can significantly improve the immune function, reduce the expression level of VEGF, improve the QoL, prolong the survival and obtain satisfactory short-term efficacy in RCC patients, which has important application value in the clinical treatment of RCC. Sorafenib 13-22 vascular endothelial growth factor A Homo sapiens 123-127 30352941-1 2019 LESSONS LEARNED: Patients with hepatocellular carcinoma (HCC) often have limited therapeutic responses to the vascular endothelial growth factor (VEGF) tyrosine kinase inhibitor sorafenib, which is standard of care in advanced HCC. Sorafenib 178-187 vascular endothelial growth factor A Homo sapiens 110-144 30962952-1 2019 Sorafenib, a multikinase inhibitor targeting the Ras/Raf/MAPK (mitogen-activated protein kinase) and vascular endothelial growth factor signaling pathways is an established treatment option for patients with advanced-stage hepatocellular carcinoma (HCC); however, despite its clinical benefit, chemoresistance and disease progression eventually occur almost invariably during treatment. Sorafenib 0-9 vascular endothelial growth factor A Homo sapiens 101-135 30935424-0 2019 Genome-wide copy number alteration and VEGFA amplification of circulating cell-free DNA as a biomarker in advanced hepatocellular carcinoma patients treated with Sorafenib. Sorafenib 162-171 vascular endothelial growth factor A Homo sapiens 39-44 30600478-7 2019 Sorafenib, a multi-kinase VEGF inhibitor, is the most widely used systemic chemotherapy approved as a first-line agent for unresectable or advanced HCC. Sorafenib 0-9 vascular endothelial growth factor A Homo sapiens 26-30 30569112-0 2019 Early decrease in serum amphiregulin or vascular endothelial growth factor levels predicts sorafenib efficacy in hepatocellular carcinoma. Sorafenib 91-100 vascular endothelial growth factor A Homo sapiens 40-74 30569112-5 2019 The aim of the present study was to investigate the effect of sorafenib on two growth factors implicated in autocrine loops and HCC tumour invasion: amphiregulin (AREG) and vascular endothelial growth factor (VEGF). Sorafenib 62-71 vascular endothelial growth factor A Homo sapiens 173-207 30569112-5 2019 The aim of the present study was to investigate the effect of sorafenib on two growth factors implicated in autocrine loops and HCC tumour invasion: amphiregulin (AREG) and vascular endothelial growth factor (VEGF). Sorafenib 62-71 vascular endothelial growth factor A Homo sapiens 209-213 30569112-8 2019 It was observed that sorafenib decreased AREG, VEGF and cytokine expression at the transcriptional and post-transcriptional levels. Sorafenib 21-30 vascular endothelial growth factor A Homo sapiens 47-51 30569112-10 2019 The decreased serum levels of AREG and VEGF after 15 days of sorafenib treatment were significantly associated with better overall and progression-free survival. Sorafenib 61-70 vascular endothelial growth factor A Homo sapiens 39-43 30569112-12 2019 These results suggest that sorafenib inhibits auto-crine loops and that early decrease in serum AREG or VEGF levels predicts sorafenib efficacy in HCC patients. Sorafenib 125-134 vascular endothelial growth factor A Homo sapiens 104-108 30352941-1 2019 LESSONS LEARNED: Patients with hepatocellular carcinoma (HCC) often have limited therapeutic responses to the vascular endothelial growth factor (VEGF) tyrosine kinase inhibitor sorafenib, which is standard of care in advanced HCC. Sorafenib 178-187 vascular endothelial growth factor A Homo sapiens 146-150 30352941-2 2019 Targeting the activin receptor-like kinase 1 (ALK1) and VEGF pathways simultaneously by combining the ALK1 ligand trap dalantercept with sorafenib may result in more effective angiogenic blockade and delay tumor progression in patients with advanced HCC.Although the combination was generally well tolerated, there was no additive antitumor activity with the combination of dalantercept plus sorafenib in patients with advanced HCC. Sorafenib 137-146 vascular endothelial growth factor A Homo sapiens 56-60 30352941-2 2019 Targeting the activin receptor-like kinase 1 (ALK1) and VEGF pathways simultaneously by combining the ALK1 ligand trap dalantercept with sorafenib may result in more effective angiogenic blockade and delay tumor progression in patients with advanced HCC.Although the combination was generally well tolerated, there was no additive antitumor activity with the combination of dalantercept plus sorafenib in patients with advanced HCC. Sorafenib 392-401 vascular endothelial growth factor A Homo sapiens 56-60 30385613-0 2019 Genetic Variants of VEGFA and FLT4 Are Determinants of Survival in Renal Cell Carcinoma Patients Treated with Sorafenib. Sorafenib 110-119 vascular endothelial growth factor A Homo sapiens 20-25 30385613-9 2019 FLT4 rs307826 and VEGFA rs58159269 led to reduced sorafenib cytotoxicity. Sorafenib 50-59 vascular endothelial growth factor A Homo sapiens 18-23 30385613-10 2019 Genetic variation in VEGFA and FLT4 could affect survival in sorafenib-treated patients with mRCC. Sorafenib 61-70 vascular endothelial growth factor A Homo sapiens 21-26 29514844-5 2018 The activation of HIF2alpha then led to the enhanced activation of VEGF, cyclin D1, and TGFalpha/EGFR pathway to mediate HCC development and reduce the sensitivity of sorafenib. Sorafenib 167-176 vascular endothelial growth factor A Homo sapiens 67-71 30369518-15 2018 And we found that 786-O RCC cells secrete high IL-6 levels after low dose stimulation with the TKIs sorafenib, sunitinib and pazopanib, inducing activation of AKT-mTOR pathway, NFkappaB, HIF-2alpha and VEGF expression. Sorafenib 100-109 vascular endothelial growth factor A Homo sapiens 202-206 30292139-5 2018 Mechanism dissection suggests that the combination of MLN8237 and sorafenib led to significant inhibition of the activation of phospho-Akt (p-Akt) and phospho-p38 mitogen-activated protein kinase (p-p38 MAPK) and their downstream genes including CDK4, cyclinD1, and VEGFA. Sorafenib 66-75 vascular endothelial growth factor A Homo sapiens 266-271 29739298-11 2018 CONCLUSIONS: Overall, our data may suggest that polymorphism analysis of the VEGF, VEGFR-2, HIF and eNOS genes can identify HCC patients who are more likely to benefit from sorafenib. Sorafenib 173-182 vascular endothelial growth factor A Homo sapiens 77-81 30378405-6 2018 Regorafenib was subsequently discontinued and the patient"s condition improved gradually, with normalization of his neurological symptoms within a month.Albeit rare, PRES has been linked to VEGF treatments, particularly sorafenib, sunitinib and pazopanib, however this is the second reported case linking regorafenib with PRES. Sorafenib 220-229 vascular endothelial growth factor A Homo sapiens 190-194 30158382-1 2018 Angiogenesis inhibitors, such as sorafenib and axitinib, which target vascular endothelial growth factor (VEGF) signaling, are widely used for renal cell carcinoma, including metastasis. Sorafenib 33-42 vascular endothelial growth factor A Homo sapiens 70-104 30158382-1 2018 Angiogenesis inhibitors, such as sorafenib and axitinib, which target vascular endothelial growth factor (VEGF) signaling, are widely used for renal cell carcinoma, including metastasis. Sorafenib 33-42 vascular endothelial growth factor A Homo sapiens 106-110 30158382-7 2018 Considering the critical role of VEGF signaling in the homeostasis of the cardiovascular system, we speculated that the long-term use of axitinib and sorafenib directly influenced the initiation of aortic dissection and cardiac dysfunction. Sorafenib 150-159 vascular endothelial growth factor A Homo sapiens 33-37 29888133-3 2018 Vascular endothelial growth factor A (VEGFA) is a crucial regulator of tumor vascularization and components of VEGF-induced cell signaling pathways are important targets of therapeutical drugs that demonstrated the highest efficiency in case of advanced HCC (sorafenib and regorafenib). Sorafenib 259-268 vascular endothelial growth factor A Homo sapiens 0-36 29888133-3 2018 Vascular endothelial growth factor A (VEGFA) is a crucial regulator of tumor vascularization and components of VEGF-induced cell signaling pathways are important targets of therapeutical drugs that demonstrated the highest efficiency in case of advanced HCC (sorafenib and regorafenib). Sorafenib 259-268 vascular endothelial growth factor A Homo sapiens 38-43 29888133-3 2018 Vascular endothelial growth factor A (VEGFA) is a crucial regulator of tumor vascularization and components of VEGF-induced cell signaling pathways are important targets of therapeutical drugs that demonstrated the highest efficiency in case of advanced HCC (sorafenib and regorafenib). Sorafenib 259-268 vascular endothelial growth factor A Homo sapiens 38-42 29703600-5 2018 VSP inhibitors include antibodies, acting extracelluarly on VEGF, such as bevacizumab and tyrosine kinases inhibitors, acting intracellularly on the kinase domain of VEGF receptors, such as sunintib and sorafenib. Sorafenib 203-212 vascular endothelial growth factor A Homo sapiens 166-170 29426804-5 2018 VEGF tyrosine kinase inhibitors (i.e. sorafenib or sunitinib) do not seem to significantly affect host"s susceptibility to infection, and universal anti-infective prophylaxis is not recommended either. Sorafenib 38-47 vascular endothelial growth factor A Homo sapiens 0-4 29620259-0 2018 Synergistic anti-hepatoma effect of bufalin combined with sorafenib via mediating the tumor vascular microenvironment by targeting mTOR/VEGF signaling. Sorafenib 58-67 vascular endothelial growth factor A Homo sapiens 136-140 29620259-13 2018 In conclusion, the results revealed a synergistic anti-hepatoma effect of bufalin combined with sorafenib via affecting the tumor vascular microenvironment by targeting mTOR/VEGF signaling. Sorafenib 96-105 vascular endothelial growth factor A Homo sapiens 174-178 29190987-10 2017 Conclusions: The findings of this study show that elderly HCC patients who relapsed after a first-line sorafenib treatment obtains a survival benefits from anti-VEGF agents rechallenge. Sorafenib 103-112 vascular endothelial growth factor A Homo sapiens 161-165 30202791-3 2018 The second wave of tyrosine kinase inhibitors (TKIs), which target the intracellular site of VEGF receptor kinases, began with the approval of sorafenib in 2005 and sunitinib in 2006. Sorafenib 143-152 vascular endothelial growth factor A Homo sapiens 93-97 29289530-9 2018 This model enables the study of anti-angiogenic drugs which target a specific factor/receptor pathway, as demonstrated by the use of the clinically approved sorafenib and sunitinib for targeting the VEGF-A/VEGFR-2 pathway. Sorafenib 157-166 vascular endothelial growth factor A Homo sapiens 199-205 29464101-1 2018 Sorafenib is a multi-kinase inhibitor and a vascular endothelial growth factor (VEGF) inhibitor approved to treat patients with advanced hepatocellular carcinoma, renal cell carcinoma and differentiated thyroid carcinoma. Sorafenib 0-9 vascular endothelial growth factor A Homo sapiens 44-78 29464101-1 2018 Sorafenib is a multi-kinase inhibitor and a vascular endothelial growth factor (VEGF) inhibitor approved to treat patients with advanced hepatocellular carcinoma, renal cell carcinoma and differentiated thyroid carcinoma. Sorafenib 0-9 vascular endothelial growth factor A Homo sapiens 80-84 28903416-7 2017 786-O RCC cells secrete high IL-6 levels after low dose stimulation with the TKIs sorafenib, sunitinib and pazopanib, inducing activation of AKT-mTOR pathway, NFkappaB, HIF-2alpha and VEGF expression. Sorafenib 82-91 vascular endothelial growth factor A Homo sapiens 184-188 27981515-0 2017 Preliminary data of VEGF-A and VEGFR-2 polymorphisms as predictive factors of radiological response and clinical outcome in iodine-refractory differentiated thyroid cancer treated with sorafenib. Sorafenib 185-194 vascular endothelial growth factor A Homo sapiens 20-26 28243971-0 2017 Erratum to: Preliminary data of VEGF-A and VEGFR-2 polymorphisms as predictive factors of radiological response and clinical outcome in iodine-refractory differentiated thyroid cancer treated with sorafenib. Sorafenib 197-206 vascular endothelial growth factor A Homo sapiens 32-38 28276433-5 2017 However, over the past decade, marked advances in the treatment of metastatic RCC have been made, with targeted agents including sorafenib, sunitinib, bevacizumab, pazopanib and axitinib, which inhibit vascular endothelial growth factor (VEGF) and its receptor (VEGFR), and everolimus and temsirolimus, which inhibit mechanistic target of rapamycin complex 1 (mTORC1), being approved. Sorafenib 129-138 vascular endothelial growth factor A Homo sapiens 202-236 28670885-0 2017 Anti-Vascular Endothelial Growth Factor Effects of Sorafenib and Arsenic Trioxide in Acute Myeloid Leukemia Cell Lines Acute myeloid leukemia (AML), is a clonal disorder caused by acquired somatic mutations and chromosomalrearrangements. Sorafenib 51-60 vascular endothelial growth factor A Homo sapiens 5-39 28670885-10 2017 The combination of sorafenib as a VEGF inhibitor withATO synergistically inhibits cell proliferation and promotes apoptosis. Sorafenib 19-28 vascular endothelial growth factor A Homo sapiens 34-38 28454454-0 2017 Chemotherapy regimen based on sorafenib combined with 5-FU on HIF-1alpha and VEGF expression and survival in advanced gastric cancer patients. Sorafenib 30-39 vascular endothelial growth factor A Homo sapiens 77-81 28454454-1 2017 The present study investigated the effect of combined sorafenib chemotherapy on hypoxia-inducible factor-1alpha (HIF-1alpha) and vascular endothelial growth factor (VEGF) expression and survival time of patients with advanced gastric cancer. Sorafenib 54-63 vascular endothelial growth factor A Homo sapiens 129-163 28454454-10 2017 After chemotherapy combined with sorafenib, the peripheral blood levels of HIF-1alpha and VEGF decreased significantly in the treatment group (P<0.05). Sorafenib 33-42 vascular endothelial growth factor A Homo sapiens 90-94 28454454-13 2017 In conclusion, chemotherapy combined with sorafenib can effectively reduce serum levels of HIF-1alpha and VEGF in patients with advanced gastric cancer, and improve their 1-year survival rate and prognosis. Sorafenib 42-51 vascular endothelial growth factor A Homo sapiens 106-110 28276433-5 2017 However, over the past decade, marked advances in the treatment of metastatic RCC have been made, with targeted agents including sorafenib, sunitinib, bevacizumab, pazopanib and axitinib, which inhibit vascular endothelial growth factor (VEGF) and its receptor (VEGFR), and everolimus and temsirolimus, which inhibit mechanistic target of rapamycin complex 1 (mTORC1), being approved. Sorafenib 129-138 vascular endothelial growth factor A Homo sapiens 238-242 27659533-0 2016 Circulating vascular endothelial growth factor (VEGF) as predictive factor of progression-free survival in patients with advanced chordoma receiving sorafenib: an analysis from a phase II trial of the french sarcoma group (GSF/GETO). Sorafenib 149-158 vascular endothelial growth factor A Homo sapiens 12-46 28105151-8 2016 In the 3-month follow-up, vascular endothelial growth factor (VEGF) levels were significantly reduced and tumor necrosis factor (TNF)-alpha levels were elevated, although the sorafenib group had significantly decreased VEGF levels and a higher TNF-alpha level than the other 2 groups (P<0.05). Sorafenib 175-184 vascular endothelial growth factor A Homo sapiens 219-223 29359059-5 2017 Four other cases of AIN reported along with inhibition of the vascular endothelial growth factor (VEGF) by either TKI (sunitinib and sorafenib) or antibodies (bevacizumab) suggest a possible class effect. Sorafenib 133-142 vascular endothelial growth factor A Homo sapiens 62-96 29359059-5 2017 Four other cases of AIN reported along with inhibition of the vascular endothelial growth factor (VEGF) by either TKI (sunitinib and sorafenib) or antibodies (bevacizumab) suggest a possible class effect. Sorafenib 133-142 vascular endothelial growth factor A Homo sapiens 98-102 27659533-0 2016 Circulating vascular endothelial growth factor (VEGF) as predictive factor of progression-free survival in patients with advanced chordoma receiving sorafenib: an analysis from a phase II trial of the french sarcoma group (GSF/GETO). Sorafenib 149-158 vascular endothelial growth factor A Homo sapiens 48-52 27659533-5 2016 During sorafenib treatment, a significant increase in PlGF (18.4 vs 43.8 pg/mL, p<0.001) was noted along with a non-significant increase in VEGF (0.7 vs 1.0 ng/mL, p=0.07). Sorafenib 7-16 vascular endothelial growth factor A Homo sapiens 143-147 27246981-6 2016 In addition, VEGF binding pathway, a druggable target by tyrosine kinase inhibitors such as sorafenib, was mutated at a higher frequency among Asians (13% vs. 2%); while the negative regulation of IL17 production, involved in inflammation and autoimmunity, was mutated only in EAs (12% vs. 0). Sorafenib 92-101 vascular endothelial growth factor A Homo sapiens 13-17 27266362-11 2016 The predominant effect of sorafenib may be through downregulation of PDGF and not VEGF. Sorafenib 26-35 vascular endothelial growth factor A Homo sapiens 82-86 27489753-6 2016 Unlike other antiangiogenic TKIs such as sunitinib or sorafenib that target vascular endothelial growth factor (VEGF) and known to cause gastrointestinal perforation, imatininib is a TKI with no known anti-VEGF activity, and so it remains unclear how imatinib would be associated with developing this life threatening complication. Sorafenib 54-63 vascular endothelial growth factor A Homo sapiens 76-110 27489753-6 2016 Unlike other antiangiogenic TKIs such as sunitinib or sorafenib that target vascular endothelial growth factor (VEGF) and known to cause gastrointestinal perforation, imatininib is a TKI with no known anti-VEGF activity, and so it remains unclear how imatinib would be associated with developing this life threatening complication. Sorafenib 54-63 vascular endothelial growth factor A Homo sapiens 112-116 26830973-8 2016 Our results suggest that polymorphisms in VEGF and VEGFR2 are associated with sorafenib clinical outcomes, and polymorphisms in VEGF and ABCB1 are associated with sorafenib-related toxicities. Sorafenib 78-87 vascular endothelial growth factor A Homo sapiens 42-46 27479949-10 2016 Treatment of EHE with VEGF inhibition, potentially in combination with other antiangiogenic and tumor-inhibiting therapies such as lenalidomide, thalidomide, sorafenib, and sunitinib, may also hold promise. Sorafenib 158-167 vascular endothelial growth factor A Homo sapiens 22-26 27034725-2 2016 Improvements in response rates and survival, with more manageable side effects compared with interleukin 2/interferon immunotherapy, have been reported with the use of targeted therapy agents, including vascular endothelial growth factor (VEGF) receptor tyrosine kinase inhibitors (sunitinib, sorafenib, pazopanib, axitinib), mammalian target of rapamycin (mTOR) inhibitors (everolimus and temsirolimus) and VEGF receptor antibodies (bevacizumab). Sorafenib 293-302 vascular endothelial growth factor A Homo sapiens 203-237 27034725-2 2016 Improvements in response rates and survival, with more manageable side effects compared with interleukin 2/interferon immunotherapy, have been reported with the use of targeted therapy agents, including vascular endothelial growth factor (VEGF) receptor tyrosine kinase inhibitors (sunitinib, sorafenib, pazopanib, axitinib), mammalian target of rapamycin (mTOR) inhibitors (everolimus and temsirolimus) and VEGF receptor antibodies (bevacizumab). Sorafenib 293-302 vascular endothelial growth factor A Homo sapiens 239-243 26667599-2 2016 We present the case of a 61-year old-man with exacerbation of pre-existing psoriasis after treatment with sorafenib, a small molecule inhibitor of the tyrosine kinase domain of the VEGF receptor, and we review the literature for other published cases of sorafenib-induced or sorafenib-exacerbated psoriasis. Sorafenib 106-115 vascular endothelial growth factor A Homo sapiens 181-185 26667599-2 2016 We present the case of a 61-year old-man with exacerbation of pre-existing psoriasis after treatment with sorafenib, a small molecule inhibitor of the tyrosine kinase domain of the VEGF receptor, and we review the literature for other published cases of sorafenib-induced or sorafenib-exacerbated psoriasis. Sorafenib 254-263 vascular endothelial growth factor A Homo sapiens 181-185 26667599-2 2016 We present the case of a 61-year old-man with exacerbation of pre-existing psoriasis after treatment with sorafenib, a small molecule inhibitor of the tyrosine kinase domain of the VEGF receptor, and we review the literature for other published cases of sorafenib-induced or sorafenib-exacerbated psoriasis. Sorafenib 254-263 vascular endothelial growth factor A Homo sapiens 181-185 26998658-1 2016 INTRODUCTION: Sorafenib is an orally available compound that acts predominantly by targeting the Ras/Raf/MEK/ERK pathway and by inhibiting the vascular endothelial growth factor (VEGF). Sorafenib 14-23 vascular endothelial growth factor A Homo sapiens 143-177 26998658-1 2016 INTRODUCTION: Sorafenib is an orally available compound that acts predominantly by targeting the Ras/Raf/MEK/ERK pathway and by inhibiting the vascular endothelial growth factor (VEGF). Sorafenib 14-23 vascular endothelial growth factor A Homo sapiens 179-183 26998658-2 2016 Since the Ras/Raf/MEK/ERK pathway is implicated in the proliferation of multiple myeloma (MM) cells and VEGF in bone marrow neovascularization, sorafenib is a drug offering the potential for targeting two important pathogenetic mechanisms involved in MM. Sorafenib 144-153 vascular endothelial growth factor A Homo sapiens 104-108 26969090-19 2016 INTERPRETATION: Adjuvant treatment with the VEGF receptor tyrosine kinase inhibitors sorafenib or sunitinib showed no survival benefit relative to placebo in a definitive phase 3 study. Sorafenib 85-94 vascular endothelial growth factor A Homo sapiens 44-48 26832420-2 2016 Oral tyrosine kinase inhibitors (TKI) targeting the VEGF receptor, including sunitinib, sorafenib, axitinib, regorafenib, pazopanib, and vandetanib reduce tumor growth and metastasis. Sorafenib 88-97 vascular endothelial growth factor A Homo sapiens 52-56 26782953-0 2016 Bufalin enhances anti-angiogenic effect of sorafenib via AKT/VEGF signaling. Sorafenib 43-52 vascular endothelial growth factor A Homo sapiens 61-65 26782953-15 2016 Taken together, our findings demonstrated for the first time that bufalin can enhance anti-angiogenic effect of sorafenib via modulating the AKT/VEGF signaling pathway. Sorafenib 112-121 vascular endothelial growth factor A Homo sapiens 145-149 26865127-3 2016 Sorafenib is a pan-VEGF receptor inhibitor, and thus many studies have focused its antivascular effects. Sorafenib 0-9 vascular endothelial growth factor A Homo sapiens 19-23 28861974-8 2016 Compared with control group, the proliferation of SK-HEP-1 cells induced by VEGF increased and and the level of NO and NOS activity induced; compared with model group, 2, 20 mumol L-1 schisantherin A and sorafenib inhibited the proliferation of SK-Hep-1 cells induced by VEGF, and reduced the level of NO and NOS activity. Sorafenib 204-213 vascular endothelial growth factor A Homo sapiens 271-275 26503994-5 2015 Sorafenib blocks platelet-derived growth factor, vascular endothelial growth factor, c-KIT and rapidly accelerated fibrosarcoma signaling, and belongs to a new class of targeted drugs. Sorafenib 0-9 vascular endothelial growth factor A Homo sapiens 49-83 26386874-3 2015 VEGF-inhibiting strategies include the use of tyrosine kinase inhibitors (sunitinib, axitinib, pazopanib, and sorafenib) and neutralizing antibodies such as bevacizumab. Sorafenib 110-119 vascular endothelial growth factor A Homo sapiens 0-4 26830973-8 2016 Our results suggest that polymorphisms in VEGF and VEGFR2 are associated with sorafenib clinical outcomes, and polymorphisms in VEGF and ABCB1 are associated with sorafenib-related toxicities. Sorafenib 78-87 vascular endothelial growth factor A Homo sapiens 51-55 28162293-3 2015 VEGF-inhibiting strategies include the use of tyrosine kinase inhibitors (sunitinib, axitinib, pazopanib, and sorafenib) and neutralizing antibodies such as bevacizumab. Sorafenib 110-119 vascular endothelial growth factor A Homo sapiens 0-4 26476711-0 2015 Prognostic Value of VEGF in Hepatocellular Carcinoma Patients Treated with Sorafenib: A Meta-Analysis. Sorafenib 75-84 vascular endothelial growth factor A Homo sapiens 20-24 26476711-3 2015 In this meta-analysis, we aimed to investigate the prognostic and predictive value of VEGF in HCC patients receiving sorafenib. Sorafenib 117-126 vascular endothelial growth factor A Homo sapiens 86-90 26476711-7 2015 RESULTS: The comprehensive search yielded 9 studies that evaluated the relationship between VEGF level and clinical outcome in advanced HCC patients treated with sorafenib. Sorafenib 162-171 vascular endothelial growth factor A Homo sapiens 92-96 26476711-9 2015 Mutation of VEGF had a favorable effect on hand-foot skin reaction in HCC patients treated with sorafenib (P<0.05). Sorafenib 96-105 vascular endothelial growth factor A Homo sapiens 12-16 26476711-10 2015 CONCLUSIONS: High level of VEGF is associated with poor outcomes in HCC patients treated with sorafenib, indicating that VEGF could be used as an indicator of clinical efficacy in patients with HCC. Sorafenib 94-103 vascular endothelial growth factor A Homo sapiens 27-31 26476711-10 2015 CONCLUSIONS: High level of VEGF is associated with poor outcomes in HCC patients treated with sorafenib, indicating that VEGF could be used as an indicator of clinical efficacy in patients with HCC. Sorafenib 94-103 vascular endothelial growth factor A Homo sapiens 121-125 26244291-6 2015 Sorafenib significantly inhibited production of TGF-beta1, VEGF, IL-6, IL-8, MCP-1, and TNF-alpha and blocked the activation of migration-related signaling molecules, such as HIF-1alpha, p-STAT3, MMP2, and Ang-1. Sorafenib 0-9 vascular endothelial growth factor A Homo sapiens 59-63 24727344-1 2015 BACKGROUND: Vascular endothelial growth factor inhibitors such as bevacizumab, sorafenib, and sunitinib are utilized in the treatment of multiple cancers. Sorafenib 79-88 vascular endothelial growth factor A Homo sapiens 12-46 26126494-1 2015 Vascular endothelial growth factor [VEGF] pathway, which plays a key role in angiogenesis, may be blocked by either extracellular interference with VEGF itself (bevacizumab [BEV] or aflibercept), or intracytoplasmic inhibition of VEGF receptor (pazopanib, nintedanib, cediranid, sunitinib and sorafenib). Sorafenib 293-302 vascular endothelial growth factor A Homo sapiens 0-34 26126494-1 2015 Vascular endothelial growth factor [VEGF] pathway, which plays a key role in angiogenesis, may be blocked by either extracellular interference with VEGF itself (bevacizumab [BEV] or aflibercept), or intracytoplasmic inhibition of VEGF receptor (pazopanib, nintedanib, cediranid, sunitinib and sorafenib). Sorafenib 293-302 vascular endothelial growth factor A Homo sapiens 36-40 26126494-1 2015 Vascular endothelial growth factor [VEGF] pathway, which plays a key role in angiogenesis, may be blocked by either extracellular interference with VEGF itself (bevacizumab [BEV] or aflibercept), or intracytoplasmic inhibition of VEGF receptor (pazopanib, nintedanib, cediranid, sunitinib and sorafenib). Sorafenib 293-302 vascular endothelial growth factor A Homo sapiens 148-152 26126494-1 2015 Vascular endothelial growth factor [VEGF] pathway, which plays a key role in angiogenesis, may be blocked by either extracellular interference with VEGF itself (bevacizumab [BEV] or aflibercept), or intracytoplasmic inhibition of VEGF receptor (pazopanib, nintedanib, cediranid, sunitinib and sorafenib). Sorafenib 293-302 vascular endothelial growth factor A Homo sapiens 148-152 26451083-3 2015 A better understanding of angiogenesis has led to the investigation of drugs that inhibit the vascular endothelial growth factor (VEGF) pathway including anti-VEGF antibody therapy (eg, bevacizumab), inhibitors of angiogenic receptor tyrosine kinases (eg, sunitinib, sorafenib, apatinib, regorafenib), and inhibitors of vascular endothelial growth factor receptors (VEGFRs) (eg, ramucirumab). Sorafenib 267-276 vascular endothelial growth factor A Homo sapiens 94-128 26451083-3 2015 A better understanding of angiogenesis has led to the investigation of drugs that inhibit the vascular endothelial growth factor (VEGF) pathway including anti-VEGF antibody therapy (eg, bevacizumab), inhibitors of angiogenic receptor tyrosine kinases (eg, sunitinib, sorafenib, apatinib, regorafenib), and inhibitors of vascular endothelial growth factor receptors (VEGFRs) (eg, ramucirumab). Sorafenib 267-276 vascular endothelial growth factor A Homo sapiens 130-134 26187792-7 2015 Furthermore, the expression of VEGF-A, VEGF-C, VEGF-D, VEGFR-2 and VEGFR-3 at protein/mRNA levels in the process of lymphatic tube formation in vitro and tumor lymphangiogenesis in vivo was downregulated; NCTD in combination with mF4-31C1 or Sorafenib enhanced these effects. Sorafenib 242-251 vascular endothelial growth factor A Homo sapiens 31-37 24823635-0 2014 Focal gains of VEGFA: candidate predictors of sorafenib response in hepatocellular carcinoma. Sorafenib 46-55 vascular endothelial growth factor A Homo sapiens 15-20 25684635-4 2015 KEY RESULTS: VEGF(165)a produced a concentration-dependent activation of the NFAT-luciferase reporter gene in living cells that was inhibited in a non-competitive fashion by four different RTKIs (cediranib, pazopanib, sorafenib and vandetanib). Sorafenib 218-227 vascular endothelial growth factor A Homo sapiens 13-17 24744262-1 2015 BACKGROUND: Sorafenib is an agent that inhibits vascular endothelial growth factor and is associated with onset or worsening of hypertension in some patients. Sorafenib 12-21 vascular endothelial growth factor A Homo sapiens 48-82 25514409-2 2014 This manuscript reviews three currently relevant anti-angiogenic agents targeting the vascular endothelial growth factor system: bevacizumab, ramucirumab and sorafenib. Sorafenib 158-167 vascular endothelial growth factor A Homo sapiens 86-120 24849467-0 2014 Autocrine vascular endothelial growth factor signaling promotes cell proliferation and modulates sorafenib treatment efficacy in hepatocellular carcinoma. Sorafenib 97-106 vascular endothelial growth factor A Homo sapiens 10-44 24849467-4 2014 Our aims were to study the molecular mechanisms underlying autocrine VEGF signaling in HCC cells and evaluate the critical role of autocrine VEGF signaling on sorafenib treatment efficacy. Sorafenib 159-168 vascular endothelial growth factor A Homo sapiens 141-145 24849467-10 2014 CONCLUSION: Autocrine VEGF signaling directly promotes HCC cell proliferation and affects the sorafenib treatment outcome in vitro and in vivo, which may enable better stratification for clinical treatment decisions. Sorafenib 94-103 vascular endothelial growth factor A Homo sapiens 22-26 24510746-2 2014 Currently, the therapeutic stronghold is sorafenib, a tyrosine kinase inhibitor (TKI) directed against the vascular endothelial growth factor (VEGF) family. Sorafenib 41-50 vascular endothelial growth factor A Homo sapiens 107-141 24510746-2 2014 Currently, the therapeutic stronghold is sorafenib, a tyrosine kinase inhibitor (TKI) directed against the vascular endothelial growth factor (VEGF) family. Sorafenib 41-50 vascular endothelial growth factor A Homo sapiens 143-147 24510746-4 2014 The aim of our study was to evaluate the role of VEGF and VEGFR polymorphisms in determining the clinical outcome of HCC patients receiving sorafenib. Sorafenib 140-149 vascular endothelial growth factor A Homo sapiens 49-53 24510746-9 2014 Once prospectively validated, the analysis of VEGF and VEGFR SNPs may represent a clinical tool to better identify HCC patients more likely to benefit from sorafenib. Sorafenib 156-165 vascular endothelial growth factor A Homo sapiens 46-50 24218035-0 2014 Low level of baseline circulating VEGF-A is associated with better outcome in patients with vascular sarcomas receiving sorafenib: an ancillary study from a phase II trial. Sorafenib 120-129 vascular endothelial growth factor A Homo sapiens 34-40 24687604-7 2014 FISH analysis of a retrospective patient cohort showed markedly improved survival of sorafenib-treated patients with VEGFA-amplified HCCs, suggesting that VEGFA amplification is a potential biomarker for HCC response to VEGF-A-blocking drugs. Sorafenib 85-94 vascular endothelial growth factor A Homo sapiens 117-122 24687604-7 2014 FISH analysis of a retrospective patient cohort showed markedly improved survival of sorafenib-treated patients with VEGFA-amplified HCCs, suggesting that VEGFA amplification is a potential biomarker for HCC response to VEGF-A-blocking drugs. Sorafenib 85-94 vascular endothelial growth factor A Homo sapiens 155-160 24687604-7 2014 FISH analysis of a retrospective patient cohort showed markedly improved survival of sorafenib-treated patients with VEGFA-amplified HCCs, suggesting that VEGFA amplification is a potential biomarker for HCC response to VEGF-A-blocking drugs. Sorafenib 85-94 vascular endothelial growth factor A Homo sapiens 220-226 25645584-13 2015 This observation may explain the higher response of agents that target vascular endothelial growth factor (such as sorafenib) in patients with VHr-HCC. Sorafenib 115-124 vascular endothelial growth factor A Homo sapiens 71-105 25895026-1 2015 Sorafenib, an oral multikinase inhibitor of Raf, VEGF and PDGF receptor signaling is approved for advanced hepatocellular carcinoma (HCC). Sorafenib 0-9 vascular endothelial growth factor A Homo sapiens 49-53 25363205-2 2015 Sorafenib, a tyrosine kinase inhibitor of vascular endothelial growth factor receptor (VEGFR), combined with bevacizumab, a monoclonal antibody to vascular endothelial growth factor (VEGF-A), would vertically inhibit VEGF/VEGFR signaling. Sorafenib 0-9 vascular endothelial growth factor A Homo sapiens 42-76 25363205-2 2015 Sorafenib, a tyrosine kinase inhibitor of vascular endothelial growth factor receptor (VEGFR), combined with bevacizumab, a monoclonal antibody to vascular endothelial growth factor (VEGF-A), would vertically inhibit VEGF/VEGFR signaling. Sorafenib 0-9 vascular endothelial growth factor A Homo sapiens 87-91 25218350-5 2014 HIF-2alpha played a dominant role in regulating VEGF, thus sorafenib in turn increased the expression of VEGF (a downstream molecule of both HIF-1 and HIF-2) and cyclin D1 (a downstream molecule of HIF-2), but reduced the expression of LDHA (a downstream molecule of HIF-1), in hypoxic HCC cells. Sorafenib 59-68 vascular endothelial growth factor A Homo sapiens 48-52 25218350-5 2014 HIF-2alpha played a dominant role in regulating VEGF, thus sorafenib in turn increased the expression of VEGF (a downstream molecule of both HIF-1 and HIF-2) and cyclin D1 (a downstream molecule of HIF-2), but reduced the expression of LDHA (a downstream molecule of HIF-1), in hypoxic HCC cells. Sorafenib 59-68 vascular endothelial growth factor A Homo sapiens 105-109 25309777-4 2014 Vascular endothelial growth factor (VEGF)- and RET-directed therapies such as sorafenib, motesanib, and sunitinib have been shown to be the most effective at inducing clinical responses and stabilizing the disease process. Sorafenib 78-87 vascular endothelial growth factor A Homo sapiens 0-34 25309777-4 2014 Vascular endothelial growth factor (VEGF)- and RET-directed therapies such as sorafenib, motesanib, and sunitinib have been shown to be the most effective at inducing clinical responses and stabilizing the disease process. Sorafenib 78-87 vascular endothelial growth factor A Homo sapiens 36-40 24817603-16 2014 CONCLUSIONS: Combined VEGF/VEGFR blockade using bevacizumab with sorafenib shows clinical activity. Sorafenib 65-74 vascular endothelial growth factor A Homo sapiens 22-26 24891362-0 2014 VEGFA genomic amplification tailors treatment of HCCs with sorafenib. Sorafenib 59-68 vascular endothelial growth factor A Homo sapiens 0-5 24891362-1 2014 In this issue of Cancer Discovery, Horwitz and colleagues identified a subtype of hepatocelluar carcinoma (HCC) bearing VEGFA genomic amplification that is particularly sensitive to VEGFA inhibition and is also more sensitive to sorafenib treatment. Sorafenib 229-238 vascular endothelial growth factor A Homo sapiens 120-125 24891362-2 2014 Taken conjointly, these data suggest that VEGFA genomic amplification can be used as a biomarker for personalized treatment of HCC with sorafenib. Sorafenib 136-145 vascular endothelial growth factor A Homo sapiens 42-47 24399106-1 2014 Sorafenib, a multi-kinase inhibitor that targets the VEGF, PDGF and BRAF pathways, has demonstrated significant clinical activity in metastatic differentiated thyroid cancer. Sorafenib 0-9 vascular endothelial growth factor A Homo sapiens 53-57 24823635-3 2014 HCC patients with VEGFA amplification are distinctly sensitive to sorafenib. Sorafenib 66-75 vascular endothelial growth factor A Homo sapiens 18-23 24611881-0 2014 Sorafenib blocks the HIF-1alpha/VEGFA pathway, inhibits tumor invasion, and induces apoptosis in hepatoma cells. Sorafenib 0-9 vascular endothelial growth factor A Homo sapiens 32-37 24611881-11 2014 Sorafenib inhibited cobalt-induced HIF-1alpha and VEGFA expression in hepatoma cells. Sorafenib 0-9 vascular endothelial growth factor A Homo sapiens 50-55 24640949-1 2014 The medical treatment of metastatic renal cell carcinoma (mRCC) has undergone a paradigm shift during the last decade with the approval of five drugs targeting vascular endothelial growth factor (VEGF) or its receptors (bevacizumab, sunitinib, sorafenib, pazopanib and axitinib) and of two drugs inhibiting the PI3K/AKT/mTOR (mammalian target of rapamycin) pathway (temsirolimus and everolimus). Sorafenib 244-253 vascular endothelial growth factor A Homo sapiens 196-200 24611881-14 2014 These results showed that sorafenib was an effective inhibitor of the HIF-1alpha/VEGFA pathway, which can provide new insight into the mechanism of its anticancer activity. Sorafenib 26-35 vascular endothelial growth factor A Homo sapiens 81-86 23833308-1 2013 PURPOSE: We hypothesized that vertical blockade of VEGF signaling by combining bevacizumab with sorafenib in patients with recurrent glioblastoma would result in a synergistic therapeutic effect. Sorafenib 96-105 vascular endothelial growth factor A Homo sapiens 51-55 24692678-4 2014 Sorafenib acts on vascular endothelial growth factor (VEGF) and on platelet-derived growth factor (PDGF) related pathways. Sorafenib 0-9 vascular endothelial growth factor A Homo sapiens 18-52 24692678-4 2014 Sorafenib acts on vascular endothelial growth factor (VEGF) and on platelet-derived growth factor (PDGF) related pathways. Sorafenib 0-9 vascular endothelial growth factor A Homo sapiens 54-58 24692678-15 2014 Furthermore, the combination of sorafenib with other multiple-kinase inhibiting agents, e.g. ABT-869, a targeted-agent mainly acting in the VEGF and PDGF pathways, should be investigated in further detail. Sorafenib 32-41 vascular endothelial growth factor A Homo sapiens 140-144 24463289-3 2014 Sorafenib is a multi-kinase inhibitor of the vascular endothelial growth factor pathway and was recently introduced as a therapy for advanced HCC. Sorafenib 0-9 vascular endothelial growth factor A Homo sapiens 45-79 24122122-0 2014 Changes in plasma vascular endothelial growth factor at 8 weeks after sorafenib administration as predictors of survival for advanced hepatocellular carcinoma. Sorafenib 70-79 vascular endothelial growth factor A Homo sapiens 18-52 24122122-2 2014 Vascular endothelial growth factor (VEGF) receptor is a sorafenib target. Sorafenib 56-65 vascular endothelial growth factor A Homo sapiens 0-34 24122122-2 2014 Vascular endothelial growth factor (VEGF) receptor is a sorafenib target. Sorafenib 56-65 vascular endothelial growth factor A Homo sapiens 36-40 24122122-10 2014 CONCLUSIONS: A plasma VEGF concentration decrease at 8 weeks after starting sorafenib treatment may predict favorable overall survival in patients with advanced HCC. Sorafenib 76-85 vascular endothelial growth factor A Homo sapiens 22-26 24418169-10 2014 There was a reduction in CD31-positive blood vessels and reduced VEGF expression, which suggested a combinational effect of sorafenib and YC-1 on angiogenesis. Sorafenib 124-133 vascular endothelial growth factor A Homo sapiens 65-69 24240178-2 2014 RECENT FINDINGS: Results of the first phase III trial of VEGF-targeted therapy (sorafenib) in DTC were presented in June 2013, and two phase III trials with VEGF and rearranged during transfection-targeted therapies (vandetanib and cabozantinib) in MTC have led to approval by US Food and Drug Administration in the past 2 years. Sorafenib 80-89 vascular endothelial growth factor A Homo sapiens 57-61 24423208-4 2014 METHODS: We used an automated, quantitative immunofluorescence-based method to determine expression levels of sorafenib targets VEGF, VEGF-R1, VEGF-R2, VEGF-R3, c-RAF, B-RAF, c-Kit, and PDGFR-beta in a cohort of 96 patients treated with sorafenib. Sorafenib 110-119 vascular endothelial growth factor A Homo sapiens 128-132 25376290-9 2014 This study also suggests the necessity of anti-angiogenic therapy, such as sorafenib, since radiotherapy increases VEGF/Plt levels, and higher levels of VEGF/Plt are associated with a poor outcome. Sorafenib 75-84 vascular endothelial growth factor A Homo sapiens 115-119 23812905-0 2013 A phase II study of combined VEGF inhibitor (bevacizumab+sorafenib) in patients with metastatic breast cancer: Hoosier Oncology Group Study BRE06-109. Sorafenib 57-66 vascular endothelial growth factor A Homo sapiens 29-33 24082917-2 2013 Currently available oral VEGF tyrosine kinase inhibitors (TKIs) approved for treatment of mRCC include sorafenib, sunitinib, pazopanib, and axitinib. Sorafenib 103-112 vascular endothelial growth factor A Homo sapiens 25-29 24649118-8 2013 Albumin concentration, the change of pharmacological signal transduction as Raf-B, vascular endothelial growth factor (VEGF), and phosphorylation of MEK1/2 or ERK1/2 were found to be decreased by sorafenib. Sorafenib 196-205 vascular endothelial growth factor A Homo sapiens 83-117 23767831-2 2013 Prior attempts to block vascular endothelial growth factor (VEGF) with sunitinib, sorafenib and thalidomide have obtained disappointing results. Sorafenib 82-91 vascular endothelial growth factor A Homo sapiens 24-58 23767831-2 2013 Prior attempts to block vascular endothelial growth factor (VEGF) with sunitinib, sorafenib and thalidomide have obtained disappointing results. Sorafenib 82-91 vascular endothelial growth factor A Homo sapiens 60-64 23839492-3 2013 RESULTS: We demonstrated that, as single agents, sunitinib, sorafenib and everolimus share similar activity in inhibiting cell proliferation, signal transduction and vascular endothelial growth factor (VEGF) secretion in different RCC models, both in vitro and in tumour xenografts. Sorafenib 60-69 vascular endothelial growth factor A Homo sapiens 166-200 23839492-3 2013 RESULTS: We demonstrated that, as single agents, sunitinib, sorafenib and everolimus share similar activity in inhibiting cell proliferation, signal transduction and vascular endothelial growth factor (VEGF) secretion in different RCC models, both in vitro and in tumour xenografts. Sorafenib 60-69 vascular endothelial growth factor A Homo sapiens 202-206 23651727-49 2013 It may therefore be worth pursuing therapies targeted directly against VEGF-A and its receptors through drugs like bevacizumab, sorafenib, sunitifib, and cediranib. Sorafenib 128-137 vascular endothelial growth factor A Homo sapiens 71-77 24621801-9 2013 Other VEGF inhibitors such as bevacizumab, sorafenib, and pazopanib also elicited significant cardiovascular toxicity with incidences ranging from 51% to 68%. Sorafenib 43-52 vascular endothelial growth factor A Homo sapiens 6-10 23054975-2 2013 Sorafenib inhibits the Raf-mitogen-activated protein kinase, vascular endothelial growth factor, and platelet-derived growth factor pathways, thus inhibiting cell growth and angiogenesis. Sorafenib 0-9 vascular endothelial growth factor A Homo sapiens 61-95 22736425-12 2013 CONCLUSIONS: Differences in the incidence of HFSR may have been caused by ethnic differences in genetic polymorphisms of the TNF-alpha, VEGF, and UGT1A9 genes, especially in relation to the expression of serum TNF-alpha after sorafenib therapy. Sorafenib 226-235 vascular endothelial growth factor A Homo sapiens 136-140 23576483-3 2013 Sorafenib, a multikinase inhibitor that blocks VEGF and PDGF signaling, was the first systemic therapy to demonstrate improved survival in patients with advanced HCC. Sorafenib 0-9 vascular endothelial growth factor A Homo sapiens 47-51 23152014-1 2012 OBJECTIVE: Sorafenib is an oral multi-kinase inhibitor of Raf-1, VEGF and PDGF receptors and others, resulting in tumor regression and anti-angiogenesis. Sorafenib 11-20 vascular endothelial growth factor A Homo sapiens 65-69 23562168-3 2013 This upregulation can theoretically be counteracted with the multikinase inhibitor sorafenib, which is thought to act directly on platelet-derived growth factor, Raf kinase, and VEGF receptors. Sorafenib 83-92 vascular endothelial growth factor A Homo sapiens 178-182 23811706-1 2013 BACKGROUND: Therapy for metastatic kidney cancer is actively evolving, particularly in the results of registration drug trials that have led to the approval of vascular endothelial growth factor pathway drugs such as sorafenib, sunitinib, pazopanib, bevacizumab, and axitinib, with focus on patients with good- or intermediate-risk criteria and clear cell histology. Sorafenib 217-226 vascular endothelial growth factor A Homo sapiens 160-194 23401018-7 2013 In conclusion, after using other VEGF inhibitor such as sunitinib, sorafenib is active and safe for the treatment of patients with advanced or metastatic RCC. Sorafenib 67-76 vascular endothelial growth factor A Homo sapiens 33-37 23571475-3 2013 Sorafenib inhibits tyrosine kinases, including receptors for vascular endothelial growth factor, which are implicated in mesothelioma pathogenesis by preclinical and clinical data. Sorafenib 0-9 vascular endothelial growth factor A Homo sapiens 61-95 23572408-7 2013 A novel VEGF receptor inhibitor, tivozanib, is expected to be approved based on improvement in PFS when compared to sorafenib in the first-line setting. Sorafenib 116-125 vascular endothelial growth factor A Homo sapiens 8-12 23714492-4 2013 Everolimus is also justified in the second-line setting, and the overall survival data for sorafenib in VEGF TKI resistant disease is impressive. Sorafenib 91-100 vascular endothelial growth factor A Homo sapiens 104-108 22981172-8 2012 Sorafenib reduced the proliferation, motility, ezrin phosphorylation, vascular endothelial growth factor release, and HIF-1alpha expression of ectopic MSC. Sorafenib 0-9 vascular endothelial growth factor A Homo sapiens 70-104 24649118-8 2013 Albumin concentration, the change of pharmacological signal transduction as Raf-B, vascular endothelial growth factor (VEGF), and phosphorylation of MEK1/2 or ERK1/2 were found to be decreased by sorafenib. Sorafenib 196-205 vascular endothelial growth factor A Homo sapiens 119-123 22327313-3 2012 Therapies targeting the VEGF pathway include bevacizumab, sorafenib, sunitinib, pazopanib, and axitinib, whereas temsirolimus and everolimus inhibit the mTOR pathway. Sorafenib 58-67 vascular endothelial growth factor A Homo sapiens 24-28 22929805-11 2012 In vivo studies further confirmed the inhibitory effect of sorafenib on the expression of HIF-1alpha and VEGF proteins, leading to a decrease in tumor vascularization and growth of the xenografts. Sorafenib 59-68 vascular endothelial growth factor A Homo sapiens 105-109 22929805-13 2012 Our preclinical data expand our understanding of sorafenib"s antiangiogenic mechanism of action by inhibiting HIF-1alpha and VEGF protein expression. Sorafenib 49-58 vascular endothelial growth factor A Homo sapiens 125-129 22263801-6 2012 Diverse anti-angiogenic drugs are under investigation, and direct targeting of this pathway can be achieved by sequestration of VEGF protein using monoclonal antibodies (bevacizumab) or engineered binding site molecules (aflibercept), blockade of the VEGF receptor-2 with monoclonal antibodies or inhibition of receptor associated tyrosine kinase with low molecular weight inhibitors (cediranib, pazopanib, sorafenib or BIBF-1120). Sorafenib 407-416 vascular endothelial growth factor A Homo sapiens 128-132 22405734-5 2012 A variety of agents, including sorafenib, sunitinib, cediranib, axitinib, motesanib, linifinib and brivanib inhibit VEGF in addition to either platelet derived growth factor (PDGF), or fibroblast derived growth factor (FGF). Sorafenib 31-40 vascular endothelial growth factor A Homo sapiens 116-120 22843888-5 2012 Moreover, pre-treatment of Caki-1 (wild-type VHL) and 786-O (mutant VHL) with HDACIs followed by sorafenib reduced cell viability synergistically via activation of caspases and downregulation of the levels of myeloid leukemia cell differentiation protein (MCL1), phospho-extracellular signal-regulated kinase (ERK), and secreted vascular endothelial growth factor (VEGF). Sorafenib 97-106 vascular endothelial growth factor A Homo sapiens 329-363 22466477-0 2012 Inhibitory activity of ranibizumab, sorafenib, and pazopanib on light-induced overexpression of platelet-derived growth factor and vascular endothelial growth factor A and the vascular endothelial growth factor A receptors 1 and 2 and neuropilin 1 and 2. Sorafenib 36-45 vascular endothelial growth factor A Homo sapiens 131-167 22466477-7 2012 RESULTS: Treatment with sorafenib or pazopanib reduced the expression of VEGF receptors 1 and 2 and neuropilin 1, and sorafenib also reduced neuropilin 2. Sorafenib 24-33 vascular endothelial growth factor A Homo sapiens 73-77 22796529-3 2012 Use of 2 distinct approaches resulted in clinical efficacy in blocking the VEGF pathway: small molecule tyrosine kinase inhibitors (sunitinib, sorafenib, axitinib, pazopanib) and the humanized anti-VEGF monoclonal antibody bevacizumab that binds circulating VEGF and prevents activation of the VEGF receptor. Sorafenib 143-152 vascular endothelial growth factor A Homo sapiens 75-79 22466477-9 2012 Sorafenib and pazopanib significantly reduced light-induced overexpression and secretion of VEGF and platelet-derived growth factor. Sorafenib 0-9 vascular endothelial growth factor A Homo sapiens 92-96 22843888-5 2012 Moreover, pre-treatment of Caki-1 (wild-type VHL) and 786-O (mutant VHL) with HDACIs followed by sorafenib reduced cell viability synergistically via activation of caspases and downregulation of the levels of myeloid leukemia cell differentiation protein (MCL1), phospho-extracellular signal-regulated kinase (ERK), and secreted vascular endothelial growth factor (VEGF). Sorafenib 97-106 vascular endothelial growth factor A Homo sapiens 365-369 21858812-1 2012 Multikinase inhibitor sorafenib inhibits proliferation and angiogenesis of tumors by suppressing the Raf/MEK/ERK signaling pathway and VEGF receptor tyrosine kinase. Sorafenib 22-31 vascular endothelial growth factor A Homo sapiens 135-139 22532265-2 2012 Multiple VEGF inhibiting orally administered tyrosine kinase inhibitors (TKIs) have been approved including sunitinib, sorafenib, pazopanib and most recently, axitinib. Sorafenib 119-128 vascular endothelial growth factor A Homo sapiens 9-13 22773582-4 2012 TPA increased the NF-kappaB activity and the expressions of MMP-9 and VEGF significantly, but its effects were suppressed by sorafenib in a dose-dependent manner. Sorafenib 125-134 vascular endothelial growth factor A Homo sapiens 70-74 22773582-0 2012 Sorafenib inhibits TPA-induced MMP-9 and VEGF expression via suppression of ERK/NF-kappaB pathway in hepatocellular carcinoma cells. Sorafenib 0-9 vascular endothelial growth factor A Homo sapiens 41-45 22773582-7 2012 Sorafenib inhibits TPA-induced MMP-9 and VEGF expressions via the suppression of ERK/NF-kappaB pathway in HCC cells. Sorafenib 0-9 vascular endothelial growth factor A Homo sapiens 41-45 21424698-9 2012 Several associations were noted between single nucleotide polymorphisms in ribonucleotide reductase, Cox-2, vascular endothelial growth factor and survival in patients treated with gemcitabine and sorafenib. Sorafenib 197-206 vascular endothelial growth factor A Homo sapiens 108-142 22585430-7 2012 Choi criteria have been recently proposed as a surrogate endpoint for efficacy and to identify patients that are good responders to VEGFR inhibitors such as sunitinib and sorafenib in advanced hepatocellular carcinoma, another disease highly addicted to angiogenesis. Sorafenib 171-180 vascular endothelial growth factor A Homo sapiens 132-137 21481584-2 2011 Everolimus is an orally administered inhibitor of the mammalian target of rapamycin that recently received approval from the European Medicines Agency for the treatment of advanced RCC that has progressed on or after treatment with vascular endothelial growth factor (VEGF)-targeted therapy, and from the United States Food and Drug Administration for treatment of advanced RCC after failure of sorafenib or sunitinib. Sorafenib 395-404 vascular endothelial growth factor A Homo sapiens 268-272 22369324-9 2012 presented retrospective data showing that retreatment with VEGF-directed targeted agents, including sunitinib, bevacizumab/interferon, dovitinib and sorafenib, was associated with a progression-free survival time of approximately 5 months. Sorafenib 149-158 vascular endothelial growth factor A Homo sapiens 59-63 22916071-1 2012 Sorafenib is a multikinase inhibitor thought to target vascular endothelial growth factor and its receptor. Sorafenib 0-9 vascular endothelial growth factor A Homo sapiens 55-89 22347360-10 2012 Sorafenib significantly increased plasma VEGF, PlGF, and SDF1alpha and decreased sVEGFR-2 levels. Sorafenib 0-9 vascular endothelial growth factor A Homo sapiens 41-45 22347360-13 2012 Sorafenib also induced changes in circulating biomarkers consistent with expected VEGF pathway blockade, despite the lack of more striking clinical activity in this small series. Sorafenib 0-9 vascular endothelial growth factor A Homo sapiens 82-86 21951737-2 2011 Four agents antagonizing vascular endothelial growth factor-mediated signaling have been approved for the treatment of metastatic RCC, including the monoclonal antibody bevacizumab and the small molecular inhibitors sunitinib, sorafenib, and pazopanib. Sorafenib 227-236 vascular endothelial growth factor A Homo sapiens 25-59 20191303-1 2011 BACKGROUND: Sorafenib is an oral multikinase inhibitor that blocks cell proliferation via the ERK pathway and angiogenesis via the VEGF pathway. Sorafenib 12-21 vascular endothelial growth factor A Homo sapiens 131-135 22034894-0 2011 Better effect of sorafenib on the rhabdoid component of a clear cell renal cell carcinoma owing to its higher level of vascular endothelial growth factor-A production. Sorafenib 17-26 vascular endothelial growth factor A Homo sapiens 119-155 22078005-2 2012 Since then, vascular endothelial growth factor (VEGF) has been identified as the most potent cytokine to induce angiogenesis and drugs targeting VEGF, principally the humanized monoclonal antibody bevacizumab and the tyrosine kinase inhibitors sunitinib and sorafenib, have proven therapeutic benefit. Sorafenib 258-267 vascular endothelial growth factor A Homo sapiens 12-46 22078005-2 2012 Since then, vascular endothelial growth factor (VEGF) has been identified as the most potent cytokine to induce angiogenesis and drugs targeting VEGF, principally the humanized monoclonal antibody bevacizumab and the tyrosine kinase inhibitors sunitinib and sorafenib, have proven therapeutic benefit. Sorafenib 258-267 vascular endothelial growth factor A Homo sapiens 48-52 22188900-2 2011 Sorafenib, a multikinase inhibitor of VEGF receptor, is effective at producing tumor responses and delaying median progression free survival in patients with cytokine refractory RCC. Sorafenib 0-9 vascular endothelial growth factor A Homo sapiens 38-42 22098229-2 2011 Currently available oral multitargeted VEGF tyrosine kinase inhibitors (TKIs) that have been approved by the US Food and Drug Administration for advanced RCC, include sunitinib, sorafenib and pazopanib. Sorafenib 178-187 vascular endothelial growth factor A Homo sapiens 39-43 21952069-18 2011 A preliminary report of the investigational VEGF receptorinhibitor axitinib gave superior PFS to sorafenib after either prior cytokine or prior sunitinib treatment. Sorafenib 97-106 vascular endothelial growth factor A Homo sapiens 44-48 21933109-1 2011 Research on the formation of new blood vessels (angiogenesis) in general and vascular endothelial growth factor (VEGF) in particular is a major focus in biomedicine and has led to the clinical approval of the monoclonal anti- VEGF antibody bevazicumab; and the second-generation multitargeted receptor kinase inhibitors (RTKIs) sorafenib, sunitinib, and pazopanib. Sorafenib 328-337 vascular endothelial growth factor A Homo sapiens 226-230 21480952-1 2011 AIMS: Reversible posterior leucoencephalopathy syndrome (RPLS) has been reported following the use of anti-vascular endothelial growth factor (VEGF) agents such as bevacizumab, sorafinib and sunitinib. Sorafenib 177-186 vascular endothelial growth factor A Homo sapiens 102-141 21331764-3 2011 A recent study showed that sorafenib, a multikinase inhibitor that acts predominantly through inhibition of Raf kinase and vascular endothelial growth factor (VEGF) and platelet-derived growth factor (PDGF) receptors, exhibited potent antitumor activity in a preclinical model of cholangiocarcinoma cells. Sorafenib 27-36 vascular endothelial growth factor A Homo sapiens 123-157 21331764-3 2011 A recent study showed that sorafenib, a multikinase inhibitor that acts predominantly through inhibition of Raf kinase and vascular endothelial growth factor (VEGF) and platelet-derived growth factor (PDGF) receptors, exhibited potent antitumor activity in a preclinical model of cholangiocarcinoma cells. Sorafenib 27-36 vascular endothelial growth factor A Homo sapiens 159-163 21487053-1 2011 Sorafenib targets the Raf/mitogen-activated protein kinase, VEGF, and platelet-derived growth factor pathways and prolongs survival patients in advanced hepatocellular carcinoma (HCC). Sorafenib 0-9 vascular endothelial growth factor A Homo sapiens 60-64 21487053-11 2011 Angiogenesis decreased after all treatments (P < 0.05), although sorafenib increased Vegf-a mRNA in liver tumors. Sorafenib 68-77 vascular endothelial growth factor A Homo sapiens 88-94 20437403-5 2011 The activation of this pathway explains the use of both VEGF and VEGF-receptor inhibitors (bevacizumab, sunitinib and sorafenib) in the therapy of advanced CCRCC. Sorafenib 118-127 vascular endothelial growth factor A Homo sapiens 65-69 21386818-6 2011 Anti-VEGF therapy with sorafenib was the first systemic therapy to demonstrate improved survival in patients with advanced-stage HCC. Sorafenib 23-32 vascular endothelial growth factor A Homo sapiens 5-9 21318618-3 2011 The tyrosine kinase inhibitors (TKIs) sorafenib, sunitinib, and pazopanib are approved by the US Food and Drug Administration for the treatment of advanced RCC; however, these multitargeted agents inhibit a wide range of kinase targets in addition to the VEGFRs, resulting in a range of adverse effects unrelated to efficient VEGF blockade. Sorafenib 38-47 vascular endothelial growth factor A Homo sapiens 255-259 21253747-4 2011 This study investigates the effects of sorafenib on light-induced overexpression of VEGF and its receptors VEGFR1 and 2 in human retinal pigment epithelial (RPE) cells. Sorafenib 39-48 vascular endothelial growth factor A Homo sapiens 84-88 21540050-8 2011 Additional broad-spectrum VEGF receptor tyrosine kinase inhibitors, such as sunitinib and sorafenib, are used in monotherapy for metastatic renal carcinoma, while sunitinib is also approved for imatinib resistant gastrointestinal stromal tumors and sorafenib for advanced stage hepatocellular carcinoma. Sorafenib 90-99 vascular endothelial growth factor A Homo sapiens 26-30 21540050-8 2011 Additional broad-spectrum VEGF receptor tyrosine kinase inhibitors, such as sunitinib and sorafenib, are used in monotherapy for metastatic renal carcinoma, while sunitinib is also approved for imatinib resistant gastrointestinal stromal tumors and sorafenib for advanced stage hepatocellular carcinoma. Sorafenib 249-258 vascular endothelial growth factor A Homo sapiens 26-30 22050750-9 2011 Other small molecule inhibitors of VEGF tyrosine kinase activity (TKIs) such as sunitinib, vandetanib and sorafenib are being tested in MBC. Sorafenib 106-115 vascular endothelial growth factor A Homo sapiens 35-39 21484496-2 2011 The first category, vascular endothelial growth factor (VEGF)-directed therapies, includes sunitinib, pazopanib, sorafenib and bevacizumab. Sorafenib 113-122 vascular endothelial growth factor A Homo sapiens 20-54 21484496-2 2011 The first category, vascular endothelial growth factor (VEGF)-directed therapies, includes sunitinib, pazopanib, sorafenib and bevacizumab. Sorafenib 113-122 vascular endothelial growth factor A Homo sapiens 56-60 21237692-3 2011 Only sorafenib, an antiangiogenic agent inhibiting the VEGF and PDGF receptors as well as MAP kinase pathway, has shown a significant benefit on patient survival. Sorafenib 5-14 vascular endothelial growth factor A Homo sapiens 55-59 20708948-3 2011 Despite the initial unimpressive clinical performance of anti-VEGF antibody (bevacizumab) as cancer monotherapy, clear improvements in clinical outcomes following combination bevacizumab and chemotherapy regimens and multi-targeted VEGF receptor tyrosine kinase inhibitors (sorafenib and sunitinib) in select tumor types have established VEGF-targeted agents as an effective means of controlling cancer growth. Sorafenib 274-283 vascular endothelial growth factor A Homo sapiens 232-236 20708948-3 2011 Despite the initial unimpressive clinical performance of anti-VEGF antibody (bevacizumab) as cancer monotherapy, clear improvements in clinical outcomes following combination bevacizumab and chemotherapy regimens and multi-targeted VEGF receptor tyrosine kinase inhibitors (sorafenib and sunitinib) in select tumor types have established VEGF-targeted agents as an effective means of controlling cancer growth. Sorafenib 274-283 vascular endothelial growth factor A Homo sapiens 232-236 21273619-2 2011 Limited clinical trial data have shown minimal activity with cytokines and chemotherapy, although small-molecule inhibitors of the vascular endothelial growth factor and platelet-derived growth factor pathways such as sunitinib and sorafenib, which are associated with significant clinical activity in clear-cell RCC (ccRCC), have been associated with a 25% response rate in chRCC. Sorafenib 232-241 vascular endothelial growth factor A Homo sapiens 131-165 20962354-0 2010 Sorafenib prevents human retinal pigment epithelium cells from light-induced overexpression of VEGF, PDGF and PlGF. Sorafenib 0-9 vascular endothelial growth factor A Homo sapiens 95-99 21637343-11 2011 This observation may be related to limited and selective success of anti-VEGF agents, such as bevacizumab and sorafenib, as monotherapy in RCC compared to other forms of cancer. Sorafenib 110-119 vascular endothelial growth factor A Homo sapiens 73-77 20163917-5 2010 In contrast, non-VEGF-related side effects are observed with agents inhibiting multiple receptor tyrosine kinases (sunitinib, sorafenib, axitinib and pazopanib) and mammalian target of rapamycin inhibitors (temsirolimus and everolimus); these include diarrhoea, skin rash, stomatitis, hand-foot skin reaction, hypothyroidism, and haematological and metabolic abnormalities. Sorafenib 126-135 vascular endothelial growth factor A Homo sapiens 17-21 20651059-10 2010 In the sorafenib cohort, VEGF levels increased at 3 and 12 weeks of treatment (both weeks P < 0.0001), whereas sVEGFR-2 (both weeks P < 0.0001) and TIMP-1 levels (P = 0.002, week 3; P = 0.006, week 12) decreased. Sorafenib 7-16 vascular endothelial growth factor A Homo sapiens 25-29 20922699-7 2010 Inhibitors of vascular endothelial growth factor (VEGF), such as bevacizumab, sunitinib, and sorafenib, interfere with angiogenesis. Sorafenib 93-102 vascular endothelial growth factor A Homo sapiens 14-48 20922699-7 2010 Inhibitors of vascular endothelial growth factor (VEGF), such as bevacizumab, sunitinib, and sorafenib, interfere with angiogenesis. Sorafenib 93-102 vascular endothelial growth factor A Homo sapiens 50-54 20922699-9 2010 Sunitinib and sorafenib are small molecules inhibiting tyrosine kinase of the intracellular domain of the VEGF receptor. Sorafenib 14-23 vascular endothelial growth factor A Homo sapiens 106-110 20570927-5 2010 RESULTS: Although sorafenib significantly inhibited tumor growth and lung metastasis, it induced a significant increase in peripheral recruitment and intratumoral infiltration of F4/80- and CD11b-positive cells, which was accompanied with elevation of colony-stimulating factor-1, stromal-derived factor 1alpha, and vascular endothelial growth factor in the tumor and elevation of plasma colony-stimulating factor-1 and mouse vascular endothelial growth factor in peripheral blood, suggesting the role of macrophages in tumor progression under sorafenib treatment. Sorafenib 18-27 vascular endothelial growth factor A Homo sapiens 281-350 20567987-1 2010 Sorafenib, a multikinase inhibitor targeting vascular endothelial growth factor (VEGF)-mediated angiogenesis, is the first drug found to prolong survival of patients with advanced hepatocellular carcinoma (HCC). Sorafenib 0-9 vascular endothelial growth factor A Homo sapiens 81-85 20570927-5 2010 RESULTS: Although sorafenib significantly inhibited tumor growth and lung metastasis, it induced a significant increase in peripheral recruitment and intratumoral infiltration of F4/80- and CD11b-positive cells, which was accompanied with elevation of colony-stimulating factor-1, stromal-derived factor 1alpha, and vascular endothelial growth factor in the tumor and elevation of plasma colony-stimulating factor-1 and mouse vascular endothelial growth factor in peripheral blood, suggesting the role of macrophages in tumor progression under sorafenib treatment. Sorafenib 18-27 vascular endothelial growth factor A Homo sapiens 316-350 20571071-4 2010 Small molecule tyrosine kinase inhibitors (TKI) targeting the VEGF receptor (i.e., sunitinib, sorafenib, and vandetanib) show activity in phase II clinical studies. Sorafenib 94-103 vascular endothelial growth factor A Homo sapiens 62-66 20166888-0 2010 Sorafenib protects human optic nerve head astrocytes from light-induced overexpression of vascular endothelial growth factor, platelet-derived growth factor, and placenta growth factor. Sorafenib 0-9 vascular endothelial growth factor A Homo sapiens 90-124 20616599-1 2010 Sorafenib, a molecular-targeted agent that inhibits tumor cell proliferation and angiogenesis by inhibiting RAF serine-threonine kinase and VEGF, PDGF, Flt-3, c-Kit receptor tyrosine kinase, was approved in Europe and North America in 2007 and in Japan on May 20, 2009. Sorafenib 0-9 vascular endothelial growth factor A Homo sapiens 140-144 20166888-10 2010 CONCLUSION: Sorafenib significantly reduced light-induced overexpression of VEGF-A, PDGF-BB, and PlGF in primary human ONHAs. Sorafenib 12-21 vascular endothelial growth factor A Homo sapiens 76-82 20658715-2 2010 Vascular endothelial growth factor (VEGF) pathway is the principle target for drugs like sunitinib, sorafenib and bevacizumab. Sorafenib 100-109 vascular endothelial growth factor A Homo sapiens 0-34 20658715-2 2010 Vascular endothelial growth factor (VEGF) pathway is the principle target for drugs like sunitinib, sorafenib and bevacizumab. Sorafenib 100-109 vascular endothelial growth factor A Homo sapiens 36-40 20179216-8 2010 As suggested by these findings, Sagopilone was combined with Bevacizumab and Sorafenib, drugs targeting vascular endothelial growth factor signaling, in Sagopilone-resistant models and, indeed, antitumor activity could be restored. Sorafenib 77-86 vascular endothelial growth factor A Homo sapiens 104-138 19944696-7 2010 Conversely, inhibition of hepatoma expressed VEGF with the receptor kinase inhibitor sorafenib or with neutralizing anti-VEGF antibodies promoted polarization and inhibited HCV entry, showing an autocrine pathway. Sorafenib 85-94 vascular endothelial growth factor A Homo sapiens 45-49 20178713-6 2010 Sorafenib works by inhibiting several receptor tyrosine kinases (RTKs), such as vascular endothelial growth factor (VEGFR) and platelet-derived growth factor receptor (PDGFR)). Sorafenib 0-9 vascular endothelial growth factor A Homo sapiens 80-114 19935717-0 2010 Sorafenib, a dual Raf kinase/vascular endothelial growth factor receptor inhibitor has significant anti-myeloma activity and synergizes with common anti-myeloma drugs. Sorafenib 0-9 vascular endothelial growth factor A Homo sapiens 29-63 19935717-3 2010 Sorafenib (Nexavar) is a novel multi-kinase inhibitor that acts predominantly through inhibition of Raf-kinase and VEGF receptor 2, offering the potential for targeting two important aspects of disease biology. Sorafenib 0-9 vascular endothelial growth factor A Homo sapiens 115-119 19935717-3 2010 Sorafenib (Nexavar) is a novel multi-kinase inhibitor that acts predominantly through inhibition of Raf-kinase and VEGF receptor 2, offering the potential for targeting two important aspects of disease biology. Sorafenib 11-18 vascular endothelial growth factor A Homo sapiens 115-119 20178713-6 2010 Sorafenib works by inhibiting several receptor tyrosine kinases (RTKs), such as vascular endothelial growth factor (VEGFR) and platelet-derived growth factor receptor (PDGFR)). Sorafenib 0-9 vascular endothelial growth factor A Homo sapiens 116-121 21067536-5 2010 Small molecular inhibitors of VEGF tyrosine kinase activity, such as sorafenib, appear promising. Sorafenib 69-78 vascular endothelial growth factor A Homo sapiens 30-34 19952730-2 2010 This is the first report of sorafenib and sunitinib, both small molecule tyrosine kinase inhibitors of vascular endothelial growth factor and platelet-derived growth factor receptors, triggering radiation recall dermatitis. Sorafenib 28-37 vascular endothelial growth factor A Homo sapiens 103-137 20031962-8 2010 However, clinical development of small molecule multi-kinase inhibitors including those targeting vascular endothelial growth factor receptors, such as vandetanib, sunitinib and sorafenib, has not been very successful. Sorafenib 178-187 vascular endothelial growth factor A Homo sapiens 98-132 21158731-4 2010 The initial pessimism about the usefulness of the antiangiogenic therapeutic approach for cancer, derived from the poor results obtained in clinical trials, turned into euphoria after the approvals of the anti-VEGF monoclonal antibody bevacizumab and the multitargeted tyrosine kinase inhibitors sunitinib, sorafenib and pazopanib. Sorafenib 307-316 vascular endothelial growth factor A Homo sapiens 210-214 19481151-1 2009 Several antiangiogenic agents, including bevacizumab, sunitinib, and sorafenib, which mainly target the VEGF signaling system, have been approved for the treatment of human cancers. Sorafenib 69-78 vascular endothelial growth factor A Homo sapiens 104-108 21036880-9 2010 After treatment with sorafenib and TACE, there was a significant decrease in the concentration of plasma vascular endothelial growth factor (VEGF) from 93 ng/l to 67 ng/l. Sorafenib 21-30 vascular endothelial growth factor A Homo sapiens 105-139 21036880-9 2010 After treatment with sorafenib and TACE, there was a significant decrease in the concentration of plasma vascular endothelial growth factor (VEGF) from 93 ng/l to 67 ng/l. Sorafenib 21-30 vascular endothelial growth factor A Homo sapiens 141-145 21789125-2 2010 Based on available phase III randomized trials, anti-VEGF agents such as sunitinib, sorafenib, bevacizumab-based therapy, and mTOR-targeted agents such as temsirolimus and everolimus have been used in the treatment armamentarium for this disease. Sorafenib 84-93 vascular endothelial growth factor A Homo sapiens 53-57 19954293-7 2009 Multiple new agents targeting the VEGF pathway have been tested and approved, including sunitinib, sorafenib and bevacizumab, with others waiting in the wings. Sorafenib 99-108 vascular endothelial growth factor A Homo sapiens 34-38 19773379-1 2009 PURPOSE: Hypertension is a mechanism-based toxicity of sorafenib and other cancer therapeutics that inhibit the vascular endothelial growth factor (VEGF) signaling pathway. Sorafenib 55-64 vascular endothelial growth factor A Homo sapiens 112-146 19773379-1 2009 PURPOSE: Hypertension is a mechanism-based toxicity of sorafenib and other cancer therapeutics that inhibit the vascular endothelial growth factor (VEGF) signaling pathway. Sorafenib 55-64 vascular endothelial growth factor A Homo sapiens 148-152 19773379-2 2009 This prospective, single-center, cohort study characterized ambulatory blood pressure monitoring as an early pharmacodynamic biomarker of VEGF signaling pathway inhibition by sorafenib. Sorafenib 175-184 vascular endothelial growth factor A Homo sapiens 138-142 19773379-8 2009 CONCLUSIONS: Ambulatory blood pressure monitoring detects the blood pressure response to VEGF signaling pathway inhibition by sorafenib during the first 24 hours of treatment. Sorafenib 126-135 vascular endothelial growth factor A Homo sapiens 89-93 19381758-3 2009 Shortly after chemotherapy with sorafenib [anti-vascular endothelial growth factor (VEGF)] was initiated, progressive renal impairment, hypertension, and nephrotic-range proteinuria developed. Sorafenib 32-41 vascular endothelial growth factor A Homo sapiens 48-82 19381758-3 2009 Shortly after chemotherapy with sorafenib [anti-vascular endothelial growth factor (VEGF)] was initiated, progressive renal impairment, hypertension, and nephrotic-range proteinuria developed. Sorafenib 32-41 vascular endothelial growth factor A Homo sapiens 84-88 19381758-6 2009 Based on the clinical course and histopathological findings we hypothesize that sorafenib may induce nephrotic-range proteinuria and renal impairment, possibly through anti-VEGF-mediated effects on the progression of IgA nephropathy. Sorafenib 80-89 vascular endothelial growth factor A Homo sapiens 173-177 19402059-2 2009 Sunitinib malate, sorafenib tosylate, bevacizumab with interferon alpha, temsirolimus, and everolimus have improved clinical outcomes in randomized phase 3 trials by inhibiting the vascular endothelial growth factor and related pathways. Sorafenib 18-27 vascular endothelial growth factor A Homo sapiens 181-215 19671760-8 2009 Thus, it is likely that soluble epoxide hydrolase inhibition contributes to the beneficial effects from the inhibition of the VEGF receptor and other kinases during treatment with sorafenib. Sorafenib 180-189 vascular endothelial growth factor A Homo sapiens 126-130 19451442-8 2009 Baseline VEGF levels correlated with Eastern Cooperative Oncology Group performance status (P < .0001), Memorial Sloan-Kettering Cancer Center score (P < .0001), and PFS and OS in univariate (PFS, P = .0013; OS, P = .0009) and multivariate (PFS, P = .0231; OS, P = .0416) analyses of placebo patients and with short OS by multivariate analysis of patients receiving sorafenib (P = .0145). Sorafenib 372-381 vascular endothelial growth factor A Homo sapiens 9-13 19451442-9 2009 Both high-VEGF (P < .01) and low-VEGF (P < .01) groups benefited from sorafenib. Sorafenib 76-85 vascular endothelial growth factor A Homo sapiens 10-14 19451442-9 2009 Both high-VEGF (P < .01) and low-VEGF (P < .01) groups benefited from sorafenib. Sorafenib 76-85 vascular endothelial growth factor A Homo sapiens 36-40 19436197-4 2009 Sorafenib is a multikinase inhibitor that targets VEGF and PDGF receptors, other kinases, as well as the serine-threonine kinase Raf. Sorafenib 0-9 vascular endothelial growth factor A Homo sapiens 50-54 19508832-4 2009 In the past year, an unprecedented number of trials have been reported using agents targeting the EGFR (erlotinib, gefitinib, cetuximab), VEGF (bevacizumab) or the VEGF receptor (sorafenib, sunitinib, cediranib), and inhibitors of both pathways (vandetanib, erlotinib, or cetuximab plus bevacizumab). Sorafenib 179-188 vascular endothelial growth factor A Homo sapiens 164-168 19277038-0 2009 Influence of bevacizumab, sunitinib and sorafenib as single agents or in combination on the inhibitory effects of VEGF on human dendritic cell differentiation from monocytes. Sorafenib 40-49 vascular endothelial growth factor A Homo sapiens 114-118 19277038-2 2009 Bevacizumab, sorafenib and sunitinib target VEGF-mediated angiogenesis and are active against several types of cancer, but their effects on the immune system are poorly understood. Sorafenib 13-22 vascular endothelial growth factor A Homo sapiens 44-48 19277038-5 2009 Bevacizumab and sorafenib, but not sunitinib, reversed the inhibitory effects of VEGF, but not of those mediated by tumour supernatants. Sorafenib 16-25 vascular endothelial growth factor A Homo sapiens 81-85 19277038-6 2009 Dendritic cells matured under the influence of VEGF expressed less human leukocyte antigen-DR (HLA-DR) and CD86, and this effect was restored by bevacizumab and sorafenib. Sorafenib 161-170 vascular endothelial growth factor A Homo sapiens 47-51 19774211-2 2009 This breakthrough in science led to the development of a variety of small molecules inhibiting the VEGF-dependent angiogenic pathway, such as sunitinib and sorafenib. Sorafenib 156-165 vascular endothelial growth factor A Homo sapiens 99-103 19496707-5 2009 It has been tested in patients with progressive disease after therapy with tyrosine kinase receptor inhibitors (sunitinib, sorafenib or both), which interfere with signaling pathways, such as the VEGF pathway. Sorafenib 123-132 vascular endothelial growth factor A Homo sapiens 196-200 19075590-4 2008 Both sunitinib and sorafenib target VEGF and PDGF receptor tyrosine kinases while bevacizumab is a monoclonal antibody to VEGF. Sorafenib 19-28 vascular endothelial growth factor A Homo sapiens 36-40 18808443-10 2008 Sorafenib blocks tumour cell proliferation by targeting Raf/MEK/ERK signalling and exerts an antiangiogenic effect by targeting VEGF receptors-2/3 and platelet derived growth factor receptor beta tyrosine kinases. Sorafenib 0-9 vascular endothelial growth factor A Homo sapiens 128-132 19255327-1 2009 PURPOSE: Based on the pivotal role of Ras-Raf-MAP-ERK signaling and vascular endothelial growth factor (VEGF) in papillary thyroid cancer (PTC), we conducted a phase II clinical trial of sorafenib targeting RAF and VEGF receptor kinases in PTC. Sorafenib 187-196 vascular endothelial growth factor A Homo sapiens 68-102 19255327-1 2009 PURPOSE: Based on the pivotal role of Ras-Raf-MAP-ERK signaling and vascular endothelial growth factor (VEGF) in papillary thyroid cancer (PTC), we conducted a phase II clinical trial of sorafenib targeting RAF and VEGF receptor kinases in PTC. Sorafenib 187-196 vascular endothelial growth factor A Homo sapiens 104-108 19255327-1 2009 PURPOSE: Based on the pivotal role of Ras-Raf-MAP-ERK signaling and vascular endothelial growth factor (VEGF) in papillary thyroid cancer (PTC), we conducted a phase II clinical trial of sorafenib targeting RAF and VEGF receptor kinases in PTC. Sorafenib 187-196 vascular endothelial growth factor A Homo sapiens 215-219 19255327-14 2009 Four of 10 paired tumor biopsies from PTC patients showed a reduction in levels of vascular endothelial growth factor receptor phosphorylation, ERK phosphorylation, and in VEGF expression during sorafenib therapy. Sorafenib 195-204 vascular endothelial growth factor A Homo sapiens 83-117 19255327-14 2009 Four of 10 paired tumor biopsies from PTC patients showed a reduction in levels of vascular endothelial growth factor receptor phosphorylation, ERK phosphorylation, and in VEGF expression during sorafenib therapy. Sorafenib 195-204 vascular endothelial growth factor A Homo sapiens 172-176 19228742-13 2009 HFSR is increased in patients treated with bevacizumab/sorafenib combination anti-VEGF therapy, and this finding is not explained by pharmacokinetic interaction between the two agents. Sorafenib 55-64 vascular endothelial growth factor A Homo sapiens 82-86 19129670-3 2008 VEGF production was inhibited by IFN-alpha alone in ACHN and SMKT-R2 cells and by sorafenib alone in ACHN, Caki-1, SMKT-R1 and SMKT-R2 cells. Sorafenib 82-91 vascular endothelial growth factor A Homo sapiens 0-4 19129670-4 2008 However, sorafenib increased VEGF production by Caki-2 cells. Sorafenib 9-18 vascular endothelial growth factor A Homo sapiens 29-33 19129670-5 2008 Interestingly, combined treatment with the two agents suppressed VEGF production by SMKT-R1 and SMKT-R2 cells more strongly than IFN-alpha or sorafenib alone. Sorafenib 142-151 vascular endothelial growth factor A Homo sapiens 65-69 19129670-9 2008 In conclusion, combined treatment with IFN-alpha and sorafenib suppressed cell proliferation and VEGF production more strongly than treatment with each agent alone in several RCC cell lines. Sorafenib 53-62 vascular endothelial growth factor A Homo sapiens 97-101 18669456-1 2008 PURPOSE: Sorafenib inhibits Raf kinase and vascular endothelial growth factor (VEGF) receptor. Sorafenib 9-18 vascular endothelial growth factor A Homo sapiens 79-83 18922106-2 2008 Sunitinib malate, sorafenib tosylate, bevacizumab +/- interferon-alfa, temsirolimus, and everolimus have improved clinical outcomes in randomized Phase III trials by inhibiting the VEGF and related pathways. Sorafenib 18-27 vascular endothelial growth factor A Homo sapiens 181-185 18852116-0 2008 Preclinical overview of sorafenib, a multikinase inhibitor that targets both Raf and VEGF and PDGF receptor tyrosine kinase signaling. Sorafenib 24-33 vascular endothelial growth factor A Homo sapiens 85-89 18854656-9 2008 Recently, a randomized placebo-controlled phase III study showed that the multikinase inhibitor sorafenib, which inhibits VEGF and Raf, significantly improves survival of patients with advanced HCC and Child A cirrhosis. Sorafenib 96-105 vascular endothelial growth factor A Homo sapiens 122-126 18618496-1 2008 BACKGROUND: Sunitinib and sorafenib are small molecules that inhibit the vascular endothelial growth factor and related receptors with substantial clinical activity reported in metastatic renal cell carcinoma (RCC). Sorafenib 26-35 vascular endothelial growth factor A Homo sapiens 73-107 18544460-7 2008 In addition, VEGF receptor tyrosine kinase inhibitors, such as sorafenib and pazopanib, are being studied in phase I/II clinical trials. Sorafenib 63-72 vascular endothelial growth factor A Homo sapiens 13-17 18520294-5 2008 Sorafenib, which is approved for the treatment of renal cell carcinoma, is a multitargeted signal transduction inhibitor that inhibits raf-kinases, VEGF receptor-2, platelet derived growth factor receptor-B, and c-kit. Sorafenib 0-9 vascular endothelial growth factor A Homo sapiens 148-152 18506667-9 2008 Small-molecule inhibitors of the VEGF receptor tyrosine kinase, such as sunitinib and sorafenib, have also shown promise in phase II trials and are being further investigated in phase III studies. Sorafenib 86-95 vascular endothelial growth factor A Homo sapiens 33-37 18241635-3 2008 We report 2 cases of recurrent exudative AMD in which oral sorafenib, a tyrosine kinase inhibitor approved for cancer, was added to intravitreal ranibizumab, an antibody to vascular endothelial growth factor. Sorafenib 59-68 vascular endothelial growth factor A Homo sapiens 173-207 18219225-2 2008 Sorafenib is a novel RAF and VEGF receptor tyrosine kinase inhibitor. Sorafenib 0-9 vascular endothelial growth factor A Homo sapiens 29-33 18035517-3 2008 Two inhibitors targeting several protein kinases, including the VEGF receptor, have increased progression-free survival in patients with metastatic RCC and are now commercially available: sunitinib (Sutent) as first-line treatment and sorafenib (Nexavar) as second-line treatment. Sorafenib 235-244 vascular endothelial growth factor A Homo sapiens 64-68 18035517-3 2008 Two inhibitors targeting several protein kinases, including the VEGF receptor, have increased progression-free survival in patients with metastatic RCC and are now commercially available: sunitinib (Sutent) as first-line treatment and sorafenib (Nexavar) as second-line treatment. Sorafenib 246-253 vascular endothelial growth factor A Homo sapiens 64-68 18265991-3 2008 Two tyrosine kinase inhibitors targeting the vascular endothelial growth factor (VEGF) receptor have been shown to improve the progression-free survival of patients in first-line (Sunitinib vs. interferon-alpha) or second-line treatment (Sorafenib vs. placebo). Sorafenib 238-247 vascular endothelial growth factor A Homo sapiens 81-85 18165617-7 2007 Small-molecule multikinase inhibitors that target VEGF receptors (sunitinib and sorafenib) have a favorable toxicity profile and can prolong time to progression and preserve quality of life when used in newly diagnosed or previously treated patients. Sorafenib 80-89 vascular endothelial growth factor A Homo sapiens 50-54 18176955-5 2008 In this respect sorafenib, an inhibitor of Raf-, VEGF- and PDGF-signalling, is the first multi-kinase inhibitor that has been approved by the FDA for the treatment of advanced HCC. Sorafenib 16-25 vascular endothelial growth factor A Homo sapiens 49-54 18615363-3 2008 The new multitargeted kinase inhibitors sorafenib (Nexavar/BAY 43-9006) and sunitinib (Sutent/SUO 11248) interfere mainly with vascular endothelial growth factor and platelet-derived growth factor pathways. Sorafenib 40-49 vascular endothelial growth factor A Homo sapiens 127-161 18615363-3 2008 The new multitargeted kinase inhibitors sorafenib (Nexavar/BAY 43-9006) and sunitinib (Sutent/SUO 11248) interfere mainly with vascular endothelial growth factor and platelet-derived growth factor pathways. Sorafenib 51-58 vascular endothelial growth factor A Homo sapiens 127-161 18615363-3 2008 The new multitargeted kinase inhibitors sorafenib (Nexavar/BAY 43-9006) and sunitinib (Sutent/SUO 11248) interfere mainly with vascular endothelial growth factor and platelet-derived growth factor pathways. Sorafenib 59-70 vascular endothelial growth factor A Homo sapiens 127-161 18192256-5 2008 Sorafenib inhibits VEGF receptors, PDGF receptors, FLT3, RAF-1, and BRAF in vitro and has been shown to prevent the growth of tumors but not to reduce tumor size. Sorafenib 0-9 vascular endothelial growth factor A Homo sapiens 19-23 16860997-3 2006 Sunitinib, sorafenib and axitinib are new agents which belong to a class of drugs called kinase inhibitors and inhibit the VEGF, platelet-derived growth factor (PDGF) and c-KIT receptor tyrosine kinases. Sorafenib 11-20 vascular endothelial growth factor A Homo sapiens 123-127 17657252-5 2007 Sunitinib, sorafenib and axitinib are kinase inhibitors that inhibit the VEGF, platelet-derived growth factor and c-kit receptor tyrosine kinases. Sorafenib 11-20 vascular endothelial growth factor A Homo sapiens 73-77 17392388-3 2007 Several anti-VEGF agents, including ligand-binding agents such as bevacizumab and the small molecule inhibitors of VEGF and related receptors such as sunitinib and sorafenib, have demonstrated clinical activity in patients with metastatic RCC. Sorafenib 164-173 vascular endothelial growth factor A Homo sapiens 13-17 17392388-3 2007 Several anti-VEGF agents, including ligand-binding agents such as bevacizumab and the small molecule inhibitors of VEGF and related receptors such as sunitinib and sorafenib, have demonstrated clinical activity in patients with metastatic RCC. Sorafenib 164-173 vascular endothelial growth factor A Homo sapiens 115-119 17317817-3 2007 Three agents targeting the VEGF pathway have shown clinical activity as monotherapy in metastatic renal cell carcinoma: the anti-VEGF monoclonal antibody, bevacizumab, and small-molecule VEGF receptor tyrosine kinase inhibitors, sorafenib and sunitinib. Sorafenib 229-238 vascular endothelial growth factor A Homo sapiens 27-31 17537667-3 2007 The validity of VEGF inhibition as a therapeutic strategy has been well supported in randomized clinical trials, as well as U.S. Food and Drug Administration approval of the VEGF antagonists bevacizumab, sunitinib malate, sorafenib, pegaptinib and ranibizumab. Sorafenib 222-231 vascular endothelial growth factor A Homo sapiens 16-20 16859583-0 2006 Clinical activity of sorafenib and sunitinib in renal cell carcinoma refractory to previous vascular endothelial growth factor-targeted therapy: two case reports. Sorafenib 21-30 vascular endothelial growth factor A Homo sapiens 92-126 17064223-6 2006 So far, three anti-VEGF inhibitors, bevacizumab, sunitinib and sorafenib, have been approved for the treatment of solid human malignancies including colorectal cancer, gastrointestinal stromal tumours and renal cell carcinoma. Sorafenib 63-72 vascular endothelial growth factor A Homo sapiens 19-23 16859583-1 2006 Sunitinib and sorafenib are multitargeted receptor tyrosine kinase inhibitors of the vascular endothelial growth factor and platelet-derived growth factor receptor families with antiangiogenic and antitumor activity in metastatic renal cell carcinoma. Sorafenib 14-23 vascular endothelial growth factor A Homo sapiens 85-119 16685460-3 2006 Bevacizumab (Avastin), Sunitinib (Sutent) and Sorafenib (Nexavar) are anti-cancer drugs targeted to VEGF signaling pathway. Sorafenib 46-55 vascular endothelial growth factor A Homo sapiens 100-104 16685460-3 2006 Bevacizumab (Avastin), Sunitinib (Sutent) and Sorafenib (Nexavar) are anti-cancer drugs targeted to VEGF signaling pathway. Sorafenib 57-64 vascular endothelial growth factor A Homo sapiens 100-104 16474853-5 2005 In addition, sorafenib demonstrated significant activity against several receptor tyrosine kinases involved in neovascularization and tumor progression, including vascular-endothelial growth factor (VEGFR)-2, VEGFR-3, platelet-derived growth factor (PDGFR)-beta Flt-3, and c-KIT. Sorafenib 13-22 vascular endothelial growth factor A Homo sapiens 163-197 18360584-3 2006 Sorafenib (BAY 43-9006) is a new agent belonging to a class of drugs called kinase inhibitors and inhibits the VEGF, platelet-derived growth factor (PDGF), and c-KIT receptor tyrosine kinases, amongst others. Sorafenib 0-9 vascular endothelial growth factor A Homo sapiens 111-115 18360584-3 2006 Sorafenib (BAY 43-9006) is a new agent belonging to a class of drugs called kinase inhibitors and inhibits the VEGF, platelet-derived growth factor (PDGF), and c-KIT receptor tyrosine kinases, amongst others. Sorafenib 11-22 vascular endothelial growth factor A Homo sapiens 111-115 16446323-1 2006 PURPOSE: BAY 43-9006 (sorafenib) is an inhibitor of Raf kinase, the vascular endothelial growth factor (VEGF) receptor-2, and angiogenesis in tumor xenografts. Sorafenib 9-20 vascular endothelial growth factor A Homo sapiens 68-102 16446323-1 2006 PURPOSE: BAY 43-9006 (sorafenib) is an inhibitor of Raf kinase, the vascular endothelial growth factor (VEGF) receptor-2, and angiogenesis in tumor xenografts. Sorafenib 9-20 vascular endothelial growth factor A Homo sapiens 104-108 16446323-1 2006 PURPOSE: BAY 43-9006 (sorafenib) is an inhibitor of Raf kinase, the vascular endothelial growth factor (VEGF) receptor-2, and angiogenesis in tumor xenografts. Sorafenib 22-31 vascular endothelial growth factor A Homo sapiens 68-102 16446323-1 2006 PURPOSE: BAY 43-9006 (sorafenib) is an inhibitor of Raf kinase, the vascular endothelial growth factor (VEGF) receptor-2, and angiogenesis in tumor xenografts. Sorafenib 22-31 vascular endothelial growth factor A Homo sapiens 104-108 16640800-2 2006 These include the small-molecule receptor tyrosine kinase (TK) inhibitors ZD6474, sorafenib, sunitinib malate, and AG-013736, all of which inhibit VEGF receptor TK activity. Sorafenib 82-91 vascular endothelial growth factor A Homo sapiens 147-151 16474853-5 2005 In addition, sorafenib demonstrated significant activity against several receptor tyrosine kinases involved in neovascularization and tumor progression, including vascular-endothelial growth factor (VEGFR)-2, VEGFR-3, platelet-derived growth factor (PDGFR)-beta Flt-3, and c-KIT. Sorafenib 13-22 vascular endothelial growth factor A Homo sapiens 199-204