PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 35562342-5 2022 Consequently, this axis activates VEGFA/VEGFR2 signaling pathway, resulting in angiogenesis and resistance of tumor cells to sunitinib in ccRCC. Sunitinib 125-134 vascular endothelial growth factor A Homo sapiens 34-39 33812180-4 2021 As a result of the inhibition that is caused by sunitinib malate agent at the receptor level, vascular endothelial growth factor (VEGF) level increases. Sunitinib 48-57 vascular endothelial growth factor A Homo sapiens 94-128 33812180-4 2021 As a result of the inhibition that is caused by sunitinib malate agent at the receptor level, vascular endothelial growth factor (VEGF) level increases. Sunitinib 48-57 vascular endothelial growth factor A Homo sapiens 130-134 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). Sunitinib 331-340 vascular endothelial growth factor A Homo sapiens 0-34 34763724-2 2021 In recent years, pneumatosis intestinalis was reported in patients undergoing cancer treatment, and some case reports exist that report that pneumatosis intestinalis occurs during administration of vascular endothelial growth factor inhibitors, such as bevacizumab and sunitinib. Sunitinib 269-278 vascular endothelial growth factor A Homo sapiens 198-232 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). Sunitinib 50-59 vascular endothelial growth factor A Homo sapiens 9-13 33863648-1 2021 BACKGROUND: Limited data exist on the clinical effectiveness of second-line (2L) vascular endothelial growth factor (receptor) targeted inhibitor (VEGF(R)i) sunitinib after first-line (1L) immuno-oncology (IO) therapy for patients with metastatic renal cell carcinoma (mRCC) in real-world settings. Sunitinib 157-166 vascular endothelial growth factor A Homo sapiens 81-145 32661119-8 2020 The most commonly used IO and VEGF-TKIs were nivolumab (66%) and sunitinib (40%). Sunitinib 65-74 vascular endothelial growth factor A Homo sapiens 30-34 32232883-1 2020 Sunitinib, a muiti-targeted receptor tyrosine kinase inhibitor including vascular endothelial growth factor, has been widely used as a first-line treatment against metastatic renal cell carcinoma (mRCC). Sunitinib 0-9 vascular endothelial growth factor A Homo sapiens 73-107 31866228-3 2020 Another class of therapeutic agents that has been implicated in TMA is the vascular endothelial growth factor (VEGF) pathway inhibitors, including the anti-VEGF monoclonal antibody bevacizumab and the VEGF receptor tyrosine kinase inhibitor sunitinib. Sunitinib 241-250 vascular endothelial growth factor A Homo sapiens 75-109 31866228-3 2020 Another class of therapeutic agents that has been implicated in TMA is the vascular endothelial growth factor (VEGF) pathway inhibitors, including the anti-VEGF monoclonal antibody bevacizumab and the VEGF receptor tyrosine kinase inhibitor sunitinib. Sunitinib 241-250 vascular endothelial growth factor A Homo sapiens 111-115 31744648-1 2020 INTRODUCTION: Sunitinib (SUN) and pazopanib (PAZ) are 2 oral tyrosine kinase inhibitors against vascular endothelial growth factor. Sunitinib 14-23 vascular endothelial growth factor A Homo sapiens 96-130 35456602-7 2022 As demonstrated by the results of inhibition on multi-receptors by Sunitinib, we confirmed that SN-38/Sunitinib co-loaded micelles to be a treatment modality that could inhibit VEGF and PDGF receptors and enhance the antitumor effect of SN-38 (p < 0.05). Sunitinib 102-111 vascular endothelial growth factor A Homo sapiens 177-181 30640790-6 2019 Sunitinib is an oral tyrosine kinase inhibitor that interacts with several angiogenesis receptors including platelet-derived growth factor receptors and VEGF receptors, and is approved for the first-line treatment in metastatic RCC. Sunitinib 0-9 vascular endothelial growth factor A Homo sapiens 153-157 31443471-5 2019 Currently vascular endothelial growth factor (VEGF) targeted therapy based on tyrosine kinase inhibitors (TKI), sunitinib and pazopanib is the alternative regimen for patients who cannot tolerate immune checkpoint inhibitors (ICI). Sunitinib 112-121 vascular endothelial growth factor A Homo sapiens 10-44 31443471-5 2019 Currently vascular endothelial growth factor (VEGF) targeted therapy based on tyrosine kinase inhibitors (TKI), sunitinib and pazopanib is the alternative regimen for patients who cannot tolerate immune checkpoint inhibitors (ICI). Sunitinib 112-121 vascular endothelial growth factor A Homo sapiens 46-50 31268155-2 2019 The Von Hippel-Lindau tumor suppressor (VHL)-hypoxia-inducible factor 1 subunit alpha (HIF1A)/hypoxia-inducible factor 2alpha (HIF2A)-vascular endothelial growth factor A (VEGFA) protein axis is involved in the development and progression of ccRCC, whereas sunitinib, a tyrosine kinase inhibitor, blocks the binding of VEGFA to its receptor. Sunitinib 257-266 vascular endothelial growth factor A Homo sapiens 134-170 31268155-8 2019 Sunitinib resistance was associated with high HIF2A and VEGFA protein levels (b=0.57 and b=0.69 for OS and PFS, respectively; P<0.001). Sunitinib 0-9 vascular endothelial growth factor A Homo sapiens 56-61 30722031-2 2019 The first VEGF inhibitors approved for mRCC were sorafenib and sunitinib. Sunitinib 63-72 vascular endothelial growth factor A Homo sapiens 10-14 31035254-7 2019 Our results showed that after treatment with sunitinib and/or IGF1, EGF and VEGF, the antiproliferative effect of sunitinib was counteracted by EGF and IGF1 but not by VEGF. Sunitinib 114-123 vascular endothelial growth factor A Homo sapiens 76-80 30109169-12 2018 The increased IL-6 may contribute to sunitinib resistance either via VEGF-mediated angiogenesis or through shifting of the Bcl2/Bax balance in favour of anti-apoptosis. Sunitinib 37-46 vascular endothelial growth factor A Homo sapiens 69-73 30648632-11 2019 CONCLUSIONS: Individualised sunitinib therapy is feasible, safe and an effective method to manage toxicity with one of the best efficacy seen for oral vascular endothelial growth factor inhibitors in metastatic renal cell carcinoma. Sunitinib 28-37 vascular endothelial growth factor A Homo sapiens 151-185 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. Sunitinib 111-120 vascular endothelial growth factor A Homo sapiens 202-206 30428867-11 2018 CONCLUSIONS: Sunitinib is a multi-targeted inhibitor of vascular endothelial growth factor (VEGF) receptors. Sunitinib 13-22 vascular endothelial growth factor A Homo sapiens 56-90 30428867-11 2018 CONCLUSIONS: Sunitinib is a multi-targeted inhibitor of vascular endothelial growth factor (VEGF) receptors. Sunitinib 13-22 vascular endothelial growth factor A Homo sapiens 92-96 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. Sunitinib 165-174 vascular endothelial growth factor A Homo sapiens 93-97 29563634-7 2018 RESULTS: Human VE-cadherin is a direct target for sunitinib which inhibits its VEGF-induced phosphorylation and cleavage on endothelial monolayer and endothelial cell migration in the 3D model. Sunitinib 50-59 vascular endothelial growth factor A Homo sapiens 79-83 29854307-8 2018 Moreover, TRC105 enhanced the inhibitory effect of Sunitinib on VEGF signaling and reduced VEGFR2-Akt-Creb activation, suggesting a molecular cooperation between the two drugs. Sunitinib 51-60 vascular endothelial growth factor A Homo sapiens 64-68 29532881-15 2018 These results suggest that the sunitinib-adapted cells switched from a VEGF-R-dependent pathway to an alternative NRP1/cMet-dependent one. Sunitinib 31-40 vascular endothelial growth factor A Homo sapiens 71-75 29095068-9 2018 HIF2A, VEGFA, VEGFR1, VEGFR2 and VEGFR3 were highly expressed in the transcriptomic ccrcc2-subtype of tumors, known to be highly sensitive to sunitinib. Sunitinib 142-151 vascular endothelial growth factor A Homo sapiens 7-12 29095068-12 2018 CONCLUSIONS: Intratumoral expression of genes involved in the HIF-VEGF-VEGFR-pro-angiogenic pathway, especially VEGFR2, is associated with favorable outcome on sunitinib in m-ccRCCs. Sunitinib 160-169 vascular endothelial growth factor A Homo sapiens 66-70 28452850-4 2017 In this study, we confirmed sunitinib induced downregulation of its targets, such as vascular endothelial growth factor, platelet-derived growth factor, and c-kit in multiple-drug-resistant nasopharyngeal carcinoma cell line CNE2/DDP and hepatoma cell line HepG2. Sunitinib 28-37 vascular endothelial growth factor A Homo sapiens 85-119 28676023-1 2018 BACKGROUND: Sunitinib, a tyrosine kinase inhibitor of vascular endothelial growth factor (VEGF), is approved for first and second line treatment of advanced renal cell carcinoma (RCC). Sunitinib 12-21 vascular endothelial growth factor A Homo sapiens 54-88 28676023-1 2018 BACKGROUND: Sunitinib, a tyrosine kinase inhibitor of vascular endothelial growth factor (VEGF), is approved for first and second line treatment of advanced renal cell carcinoma (RCC). Sunitinib 12-21 vascular endothelial growth factor A Homo sapiens 90-94 30168120-2 2018 In 2005, with the advent of vascular endothelial growth factor (VEGF) tyrosine kinase inhibitor (TKI) therapy, the standard of care shifted to agents such as sunitinib and pazopanib. Sunitinib 158-167 vascular endothelial growth factor A Homo sapiens 28-62 30168120-2 2018 In 2005, with the advent of vascular endothelial growth factor (VEGF) tyrosine kinase inhibitor (TKI) therapy, the standard of care shifted to agents such as sunitinib and pazopanib. Sunitinib 158-167 vascular endothelial growth factor A Homo sapiens 64-68 28330808-1 2017 BACKGROUND: Sunitinib, the vascular endothelial growth factor pathway inhibitor, is an established standard-of-care for advanced renal cell carcinoma (RCC). Sunitinib 12-21 vascular endothelial growth factor A Homo sapiens 27-61 28672196-2 2017 Therapeutic alternatives such as other tyrosine kinase inhibitors, VEGF inhibitors, or mTOR inhibitors emphasize the clinical need to predict the patient"s response to sunitinib therapy before treatment initiation. Sunitinib 168-177 vascular endothelial growth factor A Homo sapiens 67-71 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. Sunitinib 93-102 vascular endothelial growth factor A Homo sapiens 184-188 29345296-9 2018 Among the test agents, sunitinib and cisplatin decreased the secretion of vascular endothelial growth factor (VEGF)-A from the A549 lung cancer cells. Sunitinib 23-32 vascular endothelial growth factor A Homo sapiens 74-108 29345296-9 2018 Among the test agents, sunitinib and cisplatin decreased the secretion of vascular endothelial growth factor (VEGF)-A from the A549 lung cancer cells. Sunitinib 23-32 vascular endothelial growth factor A Homo sapiens 110-114 30636586-4 2018 We have presented that VEGF blockage in neoadjuvant setting via bevacizumab, aflibercept and sunitinib not only has revealed some promising benefits but also has shown a large negative outcome in the adjuvant trials. Sunitinib 93-102 vascular endothelial growth factor A Homo sapiens 23-27 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. Sunitinib 171-180 vascular endothelial growth factor A Homo sapiens 199-205 28978162-9 2017 Our results suggested that VEGF and VEGFR polymorphisms were associated with outcomes in sunitinib treated mRCC patients, especially VEGFR1 polymorphisms. Sunitinib 89-98 vascular endothelial growth factor A Homo sapiens 27-31 28670632-1 2017 PURPOSE: To describe the clinical course of advanced juxtapapillary retinal capillary hemangioblastomas (RCH) associated with von Hippel-Lindau (VHL) disease treated with systemic sunitinib malate, an agent that inhibits both anti-vascular endothelial growth factor and anti-platelet-derived growth factor signaling. Sunitinib 180-196 vascular endothelial growth factor A Homo sapiens 231-265 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. Sunitinib 140-149 vascular endothelial growth factor A Homo sapiens 202-236 28167241-7 2017 Sunitinib treatment reduced vessel densities and induced hypoxia in all melanoma lines, and the magnitude of the effect was associated with the gene expression and protein secretion rate of VEGF-A. Sunitinib 0-9 vascular endothelial growth factor A Homo sapiens 190-196 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. Sunitinib 140-149 vascular endothelial growth factor A Homo sapiens 238-242 27395374-1 2017 PURPOSE: To identify prognostic molecular profiles in patients with mRCC treated with sunitinib, we performed immunohistochemical analysis for VEGF and PI3K/Akt/mTOR pathway components. Sunitinib 86-95 vascular endothelial growth factor A Homo sapiens 143-147 27395374-7 2017 CONCLUSION: Immunohistochemistry for VEGF and p-mTOR proteins may discriminate patients refractory to first-line sunitinib with poor prognosis. Sunitinib 113-122 vascular endothelial growth factor A Homo sapiens 37-41 27896475-9 2017 We also highlighted the association with sunitinib-related toxicity; in particular, VEGFA polymorphism rs3025039 (CT+TT vs. CC, OR 15.3, 95% CI 2.2-102.1; P = 0.005) is associated with severe toxicity, with the presence of the variant T allele associated with a grade >=3 AE. Sunitinib 41-50 vascular endothelial growth factor A Homo sapiens 84-89 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. Sunitinib 119-128 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. Sunitinib 119-128 vascular endothelial growth factor A Homo sapiens 98-102 27633584-8 2016 Immunohistochemistry analyses found that both sunitinib (60 mg/kg) and HM-3 (3 and 48 mg/kg) decreased microvascular density and increased percent of HIF-1alpha and VEGF expressing cells. Sunitinib 46-55 vascular endothelial growth factor A Homo sapiens 165-169 28478454-8 2017 RESULTS: VEGF (50 and 100 ng/ml) significantly augmented endothelial arginine transport in a time dependent manner, an effect which was prevented by Sunitinib (2 microM), a multi targeted receptor tyrosine kinase inhibitor. Sunitinib 149-158 vascular endothelial growth factor A Homo sapiens 9-13 27718781-1 2016 BACKGROUND: Sunitinib, a vascular endothelial growth factor pathway inhibitor, is an effective treatment for metastatic renal-cell carcinoma. Sunitinib 12-21 vascular endothelial growth factor A Homo sapiens 25-59 28105174-11 2016 Thus, sunitinib confers radiosensitivity to esophageal cancer cells, which is associated with the downregulation of HIF-1alpha and VEGF expression. Sunitinib 6-15 vascular endothelial growth factor A Homo sapiens 131-135 27123883-7 2016 Potential activity of VEGF (vascular endothelial growth factor) inhibitors such as sunitinib, valatinib, and bevacizumab is suggested in small non-controlled studies and requires validation in randomized trials. Sunitinib 83-92 vascular endothelial growth factor A Homo sapiens 22-26 26755746-8 2016 Of interest, VEGF inhibition with drugs like sunitinib, applied in cancer patients, results in a PE-like syndrome, characterized by hypertension, proteinuria and renal toxicity. Sunitinib 45-54 vascular endothelial growth factor A Homo sapiens 13-17 27580750-4 2016 Discontinuation of an anti-VEGF antibody-based drug and sunitinib markedly promotes liver metastasis. Sunitinib 56-65 vascular endothelial growth factor A Homo sapiens 27-31 27123883-7 2016 Potential activity of VEGF (vascular endothelial growth factor) inhibitors such as sunitinib, valatinib, and bevacizumab is suggested in small non-controlled studies and requires validation in randomized trials. Sunitinib 83-92 vascular endothelial growth factor A Homo sapiens 28-62 27175586-2 2016 We previously reported how VEGF and VEGFR polymorphisms might have a predictive role in patients treated with first-line sunitinib. Sunitinib 121-130 vascular endothelial growth factor A Homo sapiens 27-31 26733173-6 2016 EGCG enhanced the antiproliferation and VEGF secretion-reducing effects of sunitinib in the three tested cell lines. Sunitinib 75-84 vascular endothelial growth factor A Homo sapiens 40-44 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. Sunitinib 173-182 vascular endothelial growth factor A Homo sapiens 22-26 27175586-7 2016 CONCLUSIONS: in our analysis patients with opposite polymorphisms of rs833061, rs2010963, rs699947 of VEGF A seems to have a better PFS if treated with either sunitinib or pazopanib. Sunitinib 159-168 vascular endothelial growth factor A Homo sapiens 102-108 27103123-1 2016 PURPOSE: Sirolimus, an oral mTOR inhibitor, may complement the anti-angiogenic and anti-tumor activity of sunitinib, an oral small molecule inhibitor of multiple receptor tyrosine kinases, by vertical disruption of vascular epithelial growth factor receptor (VEGFR) signaling, by reducing the compensatory production of VEGF in sunitinib-treated patients and also by directly inhibiting tumor cell proliferation. Sunitinib 106-115 vascular endothelial growth factor A Homo sapiens 259-263 27141054-7 2016 Sunitinib sensitivity correlated with vascular endothelial growth factor (VEGF) production. Sunitinib 0-9 vascular endothelial growth factor A Homo sapiens 38-72 27141054-7 2016 Sunitinib sensitivity correlated with vascular endothelial growth factor (VEGF) production. Sunitinib 0-9 vascular endothelial growth factor A Homo sapiens 74-78 27141054-11 2016 Our data show that RCC activates EC through VEGF-dependent and -independent pathways, that sunitinib sensitivity correlates with VEGF-mediated ERK activation, and that combined inhibition of VEGF/PDGF/FGF receptors is sufficient to inhibit mitogenic signaling in EC but not in fibroblasts. Sunitinib 91-100 vascular endothelial growth factor A Homo sapiens 129-133 27141054-11 2016 Our data show that RCC activates EC through VEGF-dependent and -independent pathways, that sunitinib sensitivity correlates with VEGF-mediated ERK activation, and that combined inhibition of VEGF/PDGF/FGF receptors is sufficient to inhibit mitogenic signaling in EC but not in fibroblasts. Sunitinib 91-100 vascular endothelial growth factor A Homo sapiens 129-133 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). Sunitinib 282-291 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). Sunitinib 282-291 vascular endothelial growth factor A Homo sapiens 239-243 26893877-5 2016 Sunitinib is suggested to have preventive effects on the pathogenesis of liver fibrosis and cirrhosis in vitro, via an anti-vascular endothelial growth factor and anti-platelet-derived growth factor mechanism. Sunitinib 0-9 vascular endothelial growth factor A Homo sapiens 124-158 26923603-1 2016 Autocrine VEGF signaling is critical for sustaining prostate and other cancer stem cells (CSCs), and it is a potential therapeutic target, but we observed that CSCs isolated from prostate tumors are resistant to anti-VEGF (bevacizumab) and anti-VEGFR (sunitinib) therapy. Sunitinib 252-261 vascular endothelial growth factor A Homo sapiens 10-14 26540173-6 2016 Sunitinib was the most common VEGF-targeted therapy (77%), and it was followed by sorafenib (18.4%). Sunitinib 0-9 vascular endothelial growth factor A Homo sapiens 30-34 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. Sunitinib 77-86 vascular endothelial growth factor A Homo sapiens 52-56 26386874-3 2015 VEGF-inhibiting strategies include the use of tyrosine kinase inhibitors (sunitinib, axitinib, pazopanib, and sorafenib) and neutralizing antibodies such as bevacizumab. Sunitinib 74-83 vascular endothelial growth factor A Homo sapiens 0-4 27072203-4 2016 We here review the normal physiology of vascular endothelial growth factor in the kidney, and discuss the pathogenesis, clinical and laboratory manifestations, pathological changes in the kidney, and the management of this uncommon complication of sunitinib. Sunitinib 248-257 vascular endothelial growth factor A Homo sapiens 40-74 26617188-1 2016 Over the last few years, the most recent advances of the molecular mechanisms involved in renal cell carcinoma have led to the use of new drugs targeting VEGF, such as bevacizumab plus interferon, sorafenib, sunitinib, pazopanib, and axitinib, or the mTOR, such as temsirolimus and everolimus. Sunitinib 208-217 vascular endothelial growth factor A Homo sapiens 154-158 26015515-1 2015 PURPOSE: The aim of this study was to investigate the effect of VEGF-targeted therapy (sunitinib) on molecular intratumoral heterogeneity (ITH) in metastatic clear cell renal cancer (mccRCC). Sunitinib 87-96 vascular endothelial growth factor A Homo sapiens 64-68 26108242-1 2015 AIMS AND BACKGROUND: The introduction of agents targeting vascular endothelial growth factor has radically changed the approach to metastatic renal cell carcinoma (mRCC): sunitinib and pazopanib are now the standard first-line therapy in mRCC. Sunitinib 171-180 vascular endothelial growth factor A Homo sapiens 58-92 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). Sunitinib 279-288 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). Sunitinib 279-288 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). Sunitinib 279-288 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). Sunitinib 279-288 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). Sunitinib 256-265 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). Sunitinib 256-265 vascular endothelial growth factor A Homo sapiens 130-134 26380584-7 2015 In contrast, in RCCs with FLT1 hypermethylation, proliferation inhibition was counteracted by treatment with an anti-FLT1 peptide and both VEGF-TKIs (sunitinib and axitinib). Sunitinib 150-159 vascular endothelial growth factor A Homo sapiens 139-143 26408740-12 2015 CONCLUSION: A significantly higher expression of VEGF in CRCC in comparison to healthy parenchyma can predict a better response to sunitinib. Sunitinib 131-140 vascular endothelial growth factor A Homo sapiens 49-53 26480622-9 2015 The biologic therapies for metastatic renal cell carcinoma belong to two main groups: angiogenesis inhibitors (VEGF-R inhibitors like sunitinib, sorafenib, pazopanib and axitinib), and inhibitors of the mTOR protein (everolimus and temsirolimus). Sunitinib 134-143 vascular endothelial growth factor A Homo sapiens 111-115 28162293-3 2015 VEGF-inhibiting strategies include the use of tyrosine kinase inhibitors (sunitinib, axitinib, pazopanib, and sorafenib) and neutralizing antibodies such as bevacizumab. Sunitinib 74-83 vascular endothelial growth factor A Homo sapiens 0-4 24727344-1 2015 BACKGROUND: Vascular endothelial growth factor inhibitors such as bevacizumab, sorafenib, and sunitinib are utilized in the treatment of multiple cancers. Sunitinib 94-103 vascular endothelial growth factor A Homo sapiens 12-46 25488966-2 2015 Recent placebo-controlled phase III trials of the mammalian target of rapamycin (mTOR) inhibitor everolimus and the vascular endothelial growth factor (VEGF)/platelet-derived growth factor receptor inhibitor sunitinib have noted improved progression-free survival (PFS). Sunitinib 208-217 vascular endothelial growth factor A Homo sapiens 116-150 26151457-2 2015 We investigated the efficacy of sunitinib, a multikinase VEGF inhibitor, in patients with relapsed/refractory GE/oesophageal cancer. Sunitinib 32-41 vascular endothelial growth factor A Homo sapiens 57-61 26114873-2 2015 Sunitinib is an agent that targets VEGF receptors and is considered to be a standard treatment for metastatic or unresectable clear cell RCC (ccRCC). Sunitinib 0-9 vascular endothelial growth factor A Homo sapiens 35-39 24482243-3 2014 Encouragingly, VEGF pathway targeted drugs such as bevacizumab, sunitinib and aflibercept have shown activity in certain settings. Sunitinib 64-73 vascular endothelial growth factor A Homo sapiens 15-19 25446042-2 2015 Sunitinib, a tyrosine kinase inhibitor of the VEGF receptor, has become the mainstay of treatment for these patients. Sunitinib 0-9 vascular endothelial growth factor A Homo sapiens 46-50 26788996-5 2015 Sunitinib inhibited PDGF-stimulated proliferation, migration, phosphorylation of MAPK and PI3K/Akt proteins and changes in the expression of cell-cycle regulatory proteins in vascular smooth-muscle cells as well as VEGF-stimulated endothelial cell proliferation in vitro. Sunitinib 0-9 vascular endothelial growth factor A Homo sapiens 215-219 25515134-1 2014 BACKGROUND: Sunitinib is a multi-targeted receptor tyrosine kinase inhibitor that acts against receptors for vascular endothelial growth factor and platelet-derived growth factor. Sunitinib 12-21 vascular endothelial growth factor A Homo sapiens 109-143 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. Sunitinib 104-113 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. Sunitinib 104-113 vascular endothelial growth factor A Homo sapiens 36-40 25993161-7 2015 For recurrent and aggressive tumors, inhibitors of the vascular endothelial growth factor (VEGF) pathway, such as vatalinib, bevacizumab, and sunitinib, showed signs of activity in small, uncontrolled studies, and prospective clinical studies will test the efficacy of the tetrahydroisoquinoline trabectedin and of SMO and AKT1 inhibitors. Sunitinib 142-151 vascular endothelial growth factor A Homo sapiens 55-89 25993161-7 2015 For recurrent and aggressive tumors, inhibitors of the vascular endothelial growth factor (VEGF) pathway, such as vatalinib, bevacizumab, and sunitinib, showed signs of activity in small, uncontrolled studies, and prospective clinical studies will test the efficacy of the tetrahydroisoquinoline trabectedin and of SMO and AKT1 inhibitors. Sunitinib 142-151 vascular endothelial growth factor A Homo sapiens 91-95 25085632-4 2014 METHODS: Given the preclinical evidence implicating vascular endothelial growth factor (VEGF) signaling in the biology of germ cell tumors, we hypothesized that the vascular endothelial growth factor receptor (VEGFR) inhibitor sunitinib (Sutent) may possess important clinical activity in the treatment of this refractory disease. Sunitinib 227-236 vascular endothelial growth factor A Homo sapiens 52-86 24414551-14 2014 As predicted, VEGF levels increased during sunitinib exposure followed by a rapid decline after bevacizumab. Sunitinib 43-52 vascular endothelial growth factor A Homo sapiens 14-18 24510251-4 2014 Two patients were treated with sunitinib at a standard dose (50 mg daily; 4 weeks on, 2 weeks off) after cyclophosphamide/vinblastine/dacarbazine chemotherapy, because vascular endothelial growth factor (VEGF)-positive cells were partly observed by immunohistochemical staining. Sunitinib 31-40 vascular endothelial growth factor A Homo sapiens 168-202 24510251-10 2014 In conclusion, sunitinib was effective in the treatment of malignant pheochromocytoma when VEGF-positive cells were observed in the tumor specimens. Sunitinib 15-24 vascular endothelial growth factor A Homo sapiens 91-95 24414551-1 2014 BACKGROUND: Sunitinib treatment results in a compensatory increase in plasma VEGF levels. Sunitinib 12-21 vascular endothelial growth factor A Homo sapiens 77-81 24414551-16 2014 The increase in VEGF at D42 was unexpected based on sunitinib alone and contrary to the hypothesis that we would block VEGF flare with low-dose bevacizumab. Sunitinib 52-61 vascular endothelial growth factor A Homo sapiens 16-20 24414551-2 2014 Acute withdrawal of sunitinib results in a proliferative withdrawal flare, primarily due to elevated VEGF levels. Sunitinib 20-29 vascular endothelial growth factor A Homo sapiens 101-105 24120473-14 2014 Strategies to reduce autocrine VEGF signaling (eg, with sunitinib) might be used to prevent or treat cancer in patients with Barrett"s esophagus. Sunitinib 56-65 vascular endothelial growth factor A Homo sapiens 31-35 25018885-3 2014 Autoimmune and neurological side effects have been linked to sunitinib"s inhibition of VEGF receptors with a corresponding increase in VEGF levels, which is associated with development of different neuropathies. Sunitinib 61-70 vascular endothelial growth factor A Homo sapiens 87-91 24475095-10 2014 MiR-942 overexpression in Caki-2 up-regulates MMP-9 and VEGF secretion which, in turn, promote HBMEC endothelial migration and sunitinib resistance. Sunitinib 127-136 vascular endothelial growth factor A Homo sapiens 56-60 24475095-13 2014 We describe a novel paracrine mechanism through which high miR-942 levels in MRCC cells up-regulates MMP-9 and VEGF secretion to enhance endothelial migration and sunitinib resistance. Sunitinib 163-172 vascular endothelial growth factor A Homo sapiens 111-115 24025975-1 2014 Sunitinib is a multiple tyrosine kinase inhibitor of the vascular endothelial growth factor and platelet-derived growth factor pathway and inhibits angiogenesis, cell proliferation, and tumor cell invasion, and stimulates apoptosis. Sunitinib 0-9 vascular endothelial growth factor A Homo sapiens 57-91 24018642-7 2014 Furthermore, sunitinib and rapamycin displayed synergistic activity against tube formation by human microvessel endothelial cells as well as outgrowth of endothelial tubes and microvessels both in vitro and in vivo, which is associated with down-regulation of VEGF secretion and HIF1alpha expression. Sunitinib 13-22 vascular endothelial growth factor A Homo sapiens 260-264 25018885-3 2014 Autoimmune and neurological side effects have been linked to sunitinib"s inhibition of VEGF receptors with a corresponding increase in VEGF levels, which is associated with development of different neuropathies. Sunitinib 61-70 vascular endothelial growth factor A Homo sapiens 135-139 24685916-3 2014 She was successfully treated with daily administration of sunitinib malate, an oral multi-target tyrosine kinase inhibitor, which particularly targets vascular endothelial growth factor (VEGF) receptors. Sunitinib 58-74 vascular endothelial growth factor A Homo sapiens 151-185 24685916-3 2014 She was successfully treated with daily administration of sunitinib malate, an oral multi-target tyrosine kinase inhibitor, which particularly targets vascular endothelial growth factor (VEGF) receptors. Sunitinib 58-74 vascular endothelial growth factor A Homo sapiens 187-191 24222145-0 2013 VEGF expression and response to sunitinib in patients with metastatic clear cell renal cell carcinoma. Sunitinib 32-41 vascular endothelial growth factor A Homo sapiens 0-4 26168132-4 2014 The combination of sunitinib with acriflavine significantly decreased vascular endothelial growth factor and TGF-beta expression and reduced tumor vasculature followed by increased intratumor necrosis and apoptosis. Sunitinib 19-28 vascular endothelial growth factor A Homo sapiens 70-104 24257372-0 2013 PKPD Modeling of VEGF, sVEGFR-2, sVEGFR-3, and sKIT as Predictors of Tumor Dynamics and Overall Survival Following Sunitinib Treatment in GIST. Sunitinib 115-124 vascular endothelial growth factor A Homo sapiens 17-21 24222145-5 2013 Patients with higher H-score and higher VEGF expression had a significantly shorter survival; OS after first-line sunitinib therapy and PFS correlated with MSKCC score and DMFS but not with VEGF expression and H score. Sunitinib 114-123 vascular endothelial growth factor A Homo sapiens 40-44 24222145-1 2013 AIM: To verify whether vascular endothelial growth factor (VEGF) is associated with distant metastasis free survival (DMFS) and Overall Survival (OS) of patients with renal cell carcinoma (RCC) treated with sunitinib. Sunitinib 207-216 vascular endothelial growth factor A Homo sapiens 23-57 24222145-1 2013 AIM: To verify whether vascular endothelial growth factor (VEGF) is associated with distant metastasis free survival (DMFS) and Overall Survival (OS) of patients with renal cell carcinoma (RCC) treated with sunitinib. Sunitinib 207-216 vascular endothelial growth factor A Homo sapiens 59-63 23659419-0 2013 Acute renal failure during the "off" period after sunitinib administration: possible mechanism of vascular endothelial growth factor cascade hyperactivation. Sunitinib 50-59 vascular endothelial growth factor A Homo sapiens 98-132 23475388-8 2013 CONCLUSIONS: Our findings showing constant expression levels of VEGFR2 in endothelial cells serve as a first indication that the use of small tyrosine kinase inhibitors such as Sunitinib directly targeting the VEGF-receptors might be worth testing, also in the clinical context in cases of therapy-refractory meningiomas. Sunitinib 177-186 vascular endothelial growth factor A Homo sapiens 64-68 25841679-10 2013 Biologic agents targeting the VEGF and mTOR signaling pathways, e.g., sunitinib, bevacizumab or everolimus are becoming integrated as treatments for PNET"s. Sunitinib 70-79 vascular endothelial growth factor A Homo sapiens 30-34 23767831-2 2013 Prior attempts to block vascular endothelial growth factor (VEGF) with sunitinib, sorafenib and thalidomide have obtained disappointing results. Sunitinib 71-80 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. Sunitinib 71-80 vascular endothelial growth factor A Homo sapiens 60-64 23878397-0 2013 Platelet-derived growth factor/vascular endothelial growth factor receptor inactivation by sunitinib results in Tsc1/Tsc2-dependent inhibition of TORC1. Sunitinib 91-100 vascular endothelial growth factor A Homo sapiens 31-65 23878397-1 2013 Vascular endothelial growth factor (VEGF) and platelet-derived growth factor (PDGF) receptors are implicated in development and tumorigenesis and dual inhibitors like sunitinib are prescribed for cancer treatment. Sunitinib 167-176 vascular endothelial growth factor A Homo sapiens 0-34 23878397-1 2013 Vascular endothelial growth factor (VEGF) and platelet-derived growth factor (PDGF) receptors are implicated in development and tumorigenesis and dual inhibitors like sunitinib are prescribed for cancer treatment. Sunitinib 167-176 vascular endothelial growth factor A Homo sapiens 36-40 24082917-2 2013 Currently available oral VEGF tyrosine kinase inhibitors (TKIs) approved for treatment of mRCC include sorafenib, sunitinib, pazopanib, and axitinib. Sunitinib 114-123 vascular endothelial growth factor A Homo sapiens 25-29 23942298-8 2013 The role of KIT mutation and amplification in the development of ovarian dysgerminoma and the use of Sunitinib, a receptor tyrosine kinase inhibitor with an effect on vascular endothelial growth factor, platelet-derived growth factor and KIT receptors in patients with platinum-resistant GCT, are novel promising approaches. Sunitinib 101-110 vascular endothelial growth factor A Homo sapiens 167-201 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. Sunitinib 228-237 vascular endothelial growth factor A Homo sapiens 160-194 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. Sunitinib 49-58 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. Sunitinib 49-58 vascular endothelial growth factor A Homo sapiens 202-206 23839492-5 2013 Inability by sunitinib to persistently inhibit HIF-1, VEGF and pMAPK anticipated treatment resistance in xenografted tumours. Sunitinib 13-22 vascular endothelial growth factor A Homo sapiens 54-58 23459719-3 2013 The results of clinical trials have further shown that the VEGF pathway inhibitor sunitinib and the mTOR inhibitor everolimus have efficacy in patients with advanced pancreatic NETs. Sunitinib 82-91 vascular endothelial growth factor A Homo sapiens 59-63 23522954-11 2013 Finally, we checked whether compensatory activation of VEGF signaling occurred after sunitinib addition. Sunitinib 85-94 vascular endothelial growth factor A Homo sapiens 55-59 23454556-4 2013 We performed in vitro experiments to study whether Sunitinib, a platelet-derived growth factor (PDGF) and vascular endothelial growth factor (VEGF) RTKs" inhibitor, could block both activated HSC functions and angiogenesis and thus prevent the progression of cirrhotic liver to hepatocellular carcinoma. Sunitinib 51-60 vascular endothelial growth factor A Homo sapiens 106-140 23454556-4 2013 We performed in vitro experiments to study whether Sunitinib, a platelet-derived growth factor (PDGF) and vascular endothelial growth factor (VEGF) RTKs" inhibitor, could block both activated HSC functions and angiogenesis and thus prevent the progression of cirrhotic liver to hepatocellular carcinoma. Sunitinib 51-60 vascular endothelial growth factor A Homo sapiens 142-146 23626551-0 2013 Targeting VEGF-VEGFR Pathway by Sunitinib in Peripheral Primitive Neuroectodermal Tumor, Paraganglioma and Epithelioid Hemangioendothelioma: Three Case Reports. Sunitinib 32-41 vascular endothelial growth factor A Homo sapiens 10-14 23511629-0 2013 VEGF and VEGFR polymorphisms affect clinical outcome in advanced renal cell carcinoma patients receiving first-line sunitinib. Sunitinib 116-125 vascular endothelial growth factor A Homo sapiens 0-4 22858558-2 2012 Hypertension (HTN), an on-target class effect of vascular endothelial growth factor signaling-pathway inhibitors, has been shown to correlate with clinical outcome in advanced renal cell carcinoma treated with sunitinib. Sunitinib 210-219 vascular endothelial growth factor A Homo sapiens 49-83 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). Sunitinib 42-51 vascular endothelial growth factor A Homo sapiens 116-120 23231522-1 2012 AIM: Sunitinib is an orally active multi-targeted tyrosine kinase inhibitor that exerts its antitumor effects primarily through the selective inhibition of VEGF. Sunitinib 5-14 vascular endothelial growth factor A Homo sapiens 156-160 22948895-0 2012 Polymorphisms in endothelial nitric oxide synthase (eNOS) and vascular endothelial growth factor (VEGF) predict sunitinib-induced hypertension. Sunitinib 112-121 vascular endothelial growth factor A Homo sapiens 62-96 22327313-3 2012 Therapies targeting the VEGF pathway include bevacizumab, sorafenib, sunitinib, pazopanib, and axitinib, whereas temsirolimus and everolimus inhibit the mTOR pathway. Sunitinib 69-78 vascular endothelial growth factor A Homo sapiens 24-28 22948895-0 2012 Polymorphisms in endothelial nitric oxide synthase (eNOS) and vascular endothelial growth factor (VEGF) predict sunitinib-induced hypertension. Sunitinib 112-121 vascular endothelial growth factor A Homo sapiens 98-102 22948895-7 2012 Genetic polymorphisms in VEGFA and eNOS independently predict rise in BP and/or development of severe hypertension in sunitinib-treated patients. Sunitinib 118-127 vascular endothelial growth factor A Homo sapiens 25-30 22923165-3 2012 Recently, data from two large placebo-controlled phase III trials have demonstrated that targeted therapies directed against receptor of vascular endothelial growth factor (sunitinib) and mammalian target of rapamycin (mTOR) (everolimus) produced clinically significant improvement in patients with advanced PNETs, resulting in a doubling of progression free survival and leading to their FDA approval. Sunitinib 173-182 vascular endothelial growth factor A Homo sapiens 137-171 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. Sunitinib 132-141 vascular endothelial growth factor A Homo sapiens 75-79 22515521-3 2012 Sunitinib (targeting vascular endothelial growth factor), temsirolimus (an inhibitor of the mammalian target of rapamycin - mTOR) and pazopanib (a multi-targeted receptor tyrosine kinase inhibitor) are used in the first line of recurrent disease. Sunitinib 0-9 vascular endothelial growth factor A Homo sapiens 21-55 21953673-9 2012 During sunitinib treatment, circulating Ang-2 and sTie-2 significantly decreased (p < 0.001 for both), plasma levels of sVCAM-1 and VEGF significantly increased (p = 0.022 and p < 0.001), whereas those of sICAM-1 and vWF remained stable. Sunitinib 7-16 vascular endothelial growth factor A Homo sapiens 135-139 22897944-10 2012 CONCLUSIONS: This exploratory analysis suggests that changes in sKIT and possibly VEGF-A early during sunitinib treatment may be predictive of clinical outcome in MBC. Sunitinib 102-111 vascular endothelial growth factor A Homo sapiens 82-88 21953673-13 2012 In conclusion, sunitinib-induced changes in Ang-2, sTie-2, sVCAM-1 and VEGF are related to the administration schedule, while reduction in Ang-2 is also associated with decrease in tumor burden. Sunitinib 15-24 vascular endothelial growth factor A Homo sapiens 71-75 22560921-2 2012 Sunitinib, an oral agent that inhibits the VEGF signaling pathway, may delay progression in sequence with chemotherapy. Sunitinib 0-9 vascular endothelial growth factor A Homo sapiens 43-47 22207048-12 2012 VEGF/VEGFR inhibitors, bevacizumab and sunitinib, significantly decreased the motility of pancreas cancer cells. Sunitinib 39-48 vascular endothelial growth factor A Homo sapiens 0-4 22532265-2 2012 Multiple VEGF inhibiting orally administered tyrosine kinase inhibitors (TKIs) have been approved including sunitinib, sorafenib, pazopanib and most recently, axitinib. Sunitinib 108-117 vascular endothelial growth factor A Homo sapiens 9-13 22080184-2 2012 This study aimed to assess the antitumor activity of sunitinib, a multi-targeted inhibitor of vascular endothelial growth factor receptor, c-kit, platelet-derived growth factor receptor, ret proto-oncogene (RET) and FMS-like tyrosine kinase 3 (FLT3), in ACC of the salivary gland. Sunitinib 53-62 vascular endothelial growth factor A Homo sapiens 94-128 21792888-9 2012 Sunitinib inhibited vascular endothelial growth factor (VEGF) secretion through the inhibition of STAT3 signaling and VEGF biosynthesis. Sunitinib 0-9 vascular endothelial growth factor A Homo sapiens 56-60 21792888-9 2012 Sunitinib inhibited vascular endothelial growth factor (VEGF) secretion through the inhibition of STAT3 signaling and VEGF biosynthesis. Sunitinib 0-9 vascular endothelial growth factor A Homo sapiens 118-122 22442268-1 2012 CONTEXT: Sunitinib is currently being evaluated in advanced human thyroid carcinomas, based on the rationale that the vascular endothelial growth factor and platelet-derived growth factor receptors and the RET/PTC rearrangement are valuable targets for the treatment of this malignancy. Sunitinib 9-18 vascular endothelial growth factor A Homo sapiens 118-152 22585430-3 2012 When exposed to vascular endothelial growth factor (VEGFR) inhibitors such as sunitinib, target lesions display few if any variation in tumor size, but rather detectable modifications in tumor density. Sunitinib 78-87 vascular endothelial growth factor A Homo sapiens 16-50 22585430-3 2012 When exposed to vascular endothelial growth factor (VEGFR) inhibitors such as sunitinib, target lesions display few if any variation in tumor size, but rather detectable modifications in tumor density. Sunitinib 78-87 vascular endothelial growth factor A Homo sapiens 52-57 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. Sunitinib 157-166 vascular endothelial growth factor A Homo sapiens 132-137 22314934-0 2012 Antitumor effect of vascular endothelial growth factor inhibitor sunitinib in preclinical models of hepatocellular carcinoma. Sunitinib 65-74 vascular endothelial growth factor A Homo sapiens 20-54 22314934-4 2012 Recently, another VEGF inhibitor, sunitinib, showed survival benefits in HCC hepatitis B-positive patients, but failed to improve survival in HCC hepatitis C-positive patients. Sunitinib 34-43 vascular endothelial growth factor A Homo sapiens 18-22 22344606-4 2012 We hypothesized that sunitinib would be effective in bladder cancer as it is an oral inhibitor of multiple receptor tyrosine kinases, including VEGF receptors, platelet derived growth factor (PDGF) receptors and stem cell factor receptor (c-KIT), and is a standard first-line treatment of advanced clear cell renal carcinoma. Sunitinib 21-30 vascular endothelial growth factor A Homo sapiens 168-172 21882181-5 2012 RESULTS: VEGF SNP -634 genotype was associated with the prevalence and duration of sunitinib-induced hypertension (as defined by systolic pressure >=150 mmHg and/or diastolic pressure >=90 mmHg) in both univariable analysis (P = .03 and .01, respectively) and multivariable analysis, which adjusted for baseline BP and use of antihypertension medication (P = .05 and .02, respectively). Sunitinib 83-92 vascular endothelial growth factor A Homo sapiens 9-13 21882181-9 2012 CONCLUSIONS: In MCCRCC patients treated with sunitinib, VEGF SNP -634 is associated with hypertension and a combination of VEGF SNP 936 and VEGFR2 SNP 889 genotypes is associated with overall survival. Sunitinib 45-54 vascular endothelial growth factor A Homo sapiens 56-60 22179104-1 2012 PURPOSE: Sunitinib is an oral tyrosine kinase inhibitor of VEGF, PDGF, c-KIT, and flt-3 receptors. Sunitinib 9-18 vascular endothelial growth factor A Homo sapiens 59-63 21898375-2 2012 Everolimus, an oral mTOR inhibitor, and sunitinib, an oral tyrosine kinase inhibitor targeting VEGF, are standard agents in the management of metastatic RCC. Sunitinib 40-49 vascular endothelial growth factor A Homo sapiens 95-99 20960028-1 2012 BACKGROUND: Sunitinib is an oral multitargeted tyrosine kinase inhibitor of vascular endothelial growth factor and platelet-derived growth factor receptors, as well as of other receptor types. Sunitinib 12-21 vascular endothelial growth factor A Homo sapiens 76-110 25806151-3 2012 Thus, this system has become the focus of therapeutic interventions, which led to the approval of the anti-VEGF blocking antibody bevacizumab and the VEGFR-2 pathway inhibitors pazopanib, sorafenib and sunitinib. Sunitinib 202-211 vascular endothelial growth factor A Homo sapiens 107-111 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. Sunitinib 100-109 vascular endothelial growth factor A Homo sapiens 59-63 22357730-5 2012 Specifically, phase III studies indicate that pharmacologic inhibition of the vascular endothelial growth factor pathway with sunitinib, and of the mammalian target of rapamycin pathway with everolimus, appears to have altered the natural history of these diseases. Sunitinib 126-135 vascular endothelial growth factor A Homo sapiens 78-112 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. Sunitinib 244-253 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. Sunitinib 244-253 vascular endothelial growth factor A Homo sapiens 48-52 22497103-15 2012 Sunitinib, recommended by NICE, is administered orally and acts by inhibiting the VEGF receptor. Sunitinib 0-9 vascular endothelial growth factor A Homo sapiens 82-86 21699503-2 2012 Indolinones (e.g. SU5416 and Sutent) and anilinophthalazines (e.g. PTK787) are potent small molecule inhibitors of VEGFR2 and other tyrosine kinases, but their effects on VEGF-A- and bFGF-stimulated endothelial responses are unclear. Sunitinib 29-35 vascular endothelial growth factor A Homo sapiens 171-177 21876693-4 2012 Research on angiogenesis in general, and vascular endothelial growth factor in particular, is a major focus in biomedicine and has led to the clinical approval of several antiangiogenic agents including thalidomide, bevacizumab, sorafenib, sunitinib, pazopanib, temesirolimus, and everolimus. Sunitinib 240-249 vascular endothelial growth factor A Homo sapiens 41-75 21961001-3 2012 On this basis, agents rendering VEGF ineffective by neutralizing VEGF (bevacizumab), blocking its receptors (aflibercept), or interfering with the postreceptor signaling pathways (sunitinib) provide us with the rational treatment options. Sunitinib 180-189 vascular endothelial growth factor A Homo sapiens 32-36 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. Sunitinib 167-176 vascular endothelial growth factor A Homo sapiens 39-43 21931979-4 2011 Initially developed for its inhibition of the vascular endothelial growth factor (VEGF) signaling pathway, sunitinib has been associated with hypertension and heart failure. Sunitinib 107-116 vascular endothelial growth factor A Homo sapiens 46-80 21931979-4 2011 Initially developed for its inhibition of the vascular endothelial growth factor (VEGF) signaling pathway, sunitinib has been associated with hypertension and heart failure. Sunitinib 107-116 vascular endothelial growth factor A Homo sapiens 82-86 22038997-10 2011 Sunitinib PK and VEGF ligand levels increased during sunitinib exposure and returned toward baseline during the treatment withdrawal. Sunitinib 53-62 vascular endothelial growth factor A Homo sapiens 17-21 20676744-0 2011 VEGF pathway inhibition by anticancer agent sunitinib and susceptibility to atherosclerosis plaque disruption. Sunitinib 44-53 vascular endothelial growth factor A Homo sapiens 0-4 20676744-3 2011 We report on a case of bowel infarction in a renal cancer patient treated with the anti-VEGF agent sunitinib. Sunitinib 99-108 vascular endothelial growth factor A Homo sapiens 88-92 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. Sunitinib 144-153 vascular endothelial growth factor A Homo sapiens 44-48 22005473-5 2011 METHODS: This open-labeled phase II trial evaluated single-agent sunitinib, an inhibitor of multiple receptor tyrosine kinases including the vascular endothelial growth factor receptors, given at 50 mg daily orally for 4 weeks followed by a 2-week rest, in patients with advanced MPM. Sunitinib 65-74 vascular endothelial growth factor A Homo sapiens 141-175 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. Sunitinib 339-348 vascular endothelial growth factor A Homo sapiens 226-230 21954449-12 2011 DISCUSSION: Sunitinib is a small molecule that inhibits multiple receptor tyrosine kinases such as stem cell factor receptor, vascular endothelial growth factor, and platelet-derived growth factor. Sunitinib 12-21 vascular endothelial growth factor A Homo sapiens 126-160 21672194-7 2011 A number of biologically targeted agents targeting the VEGF and mTOR signaling pathways have recently shown promise, with recent trials showing treatment with the VEGFR tyrosine kinase inhibitor sunitinib or the mTOR inhibitor everolimus improves progression-free survival in patients with advanced NET. Sunitinib 195-204 vascular endothelial growth factor A Homo sapiens 55-59 21693010-6 2011 METHODS: The effects of sunitinib on the degree of phosphorylation of VEGFR-2/3 and other signaling molecules was examined in lymphatic endothelial cells (LECs) treated with the drug; VEGF-induced LEC growth, migration, and tube formation were also examined. Sunitinib 24-33 vascular endothelial growth factor A Homo sapiens 70-74 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. Sunitinib 216-225 vascular endothelial growth factor A Homo sapiens 25-59 22040503-1 2011 BACKGROUND: The tyrosine kinase inhibitors (TKIs) sunitinib, the first targeted agent for the first line treatment of metastatic renal cell carcinoma (RCC), targets the vascular endothelial growth factor (VEGF) pathway. Sunitinib 50-59 vascular endothelial growth factor A Homo sapiens 169-203 22040503-1 2011 BACKGROUND: The tyrosine kinase inhibitors (TKIs) sunitinib, the first targeted agent for the first line treatment of metastatic renal cell carcinoma (RCC), targets the vascular endothelial growth factor (VEGF) pathway. Sunitinib 50-59 vascular endothelial growth factor A Homo sapiens 205-209 21817899-0 2011 VEGF expression is related to good response and long progression-free survival in gastrointestinal stromal tumor patients treated with Sunitinib. Sunitinib 135-144 vascular endothelial growth factor A Homo sapiens 0-4 21817899-8 2011 In the sunitinib treatment, VEGF expression was related to a favorable response (P=0.002) and long PFS (P=0.020) in univariate analysis. Sunitinib 7-16 vascular endothelial growth factor A Homo sapiens 28-32 21817899-11 2011 In conclusion, expressions of VEGF, PDGFR, and CD34 may have predictive value in sunitinib treatments. Sunitinib 81-90 vascular endothelial growth factor A Homo sapiens 30-34 21787417-11 2011 CONCLUSIONS: Baseline plasma VEGF-C levels predicted disease control (based on RECIST) and were positively associated with both TTP and OS in this exploratory analysis, suggesting that this VEGF family member may have utility in predicting clinical outcome in patients with HCC who receive sunitinib. Sunitinib 290-299 vascular endothelial growth factor A Homo sapiens 29-33 21772092-7 2011 Those patients who presented low serum VEGF showed prolonged progression-free survival when treated with sunitinib. Sunitinib 105-114 vascular endothelial growth factor A Homo sapiens 39-43 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. Sunitinib 408-417 vascular endothelial growth factor A Homo sapiens 268-272 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. Sunitinib 191-200 vascular endothelial growth factor A Homo sapiens 102-141 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. Sunitinib 191-200 vascular endothelial growth factor A Homo sapiens 143-147 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. Sunitinib 104-113 vascular endothelial growth factor A Homo sapiens 56-60 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. Sunitinib 104-113 vascular endothelial growth factor A Homo sapiens 65-69 21527770-1 2011 BACKGROUND: Hypertension (HTN) is an on-target effect of the vascular endothelial growth factor pathway inhibitor, sunitinib. Sunitinib 115-124 vascular endothelial growth factor A Homo sapiens 61-95 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. Sunitinib 76-85 vascular endothelial growth factor A Homo sapiens 26-30 21057538-1 2011 The vascular endothelial growth factor (VEGF) receptor tyrosine kinase inhibitor sunitinib has been approved for first-line treatment of patients with metastatic renal cancer and is currently being trialled in other cancers. Sunitinib 81-90 vascular endothelial growth factor A Homo sapiens 4-38 21057538-1 2011 The vascular endothelial growth factor (VEGF) receptor tyrosine kinase inhibitor sunitinib has been approved for first-line treatment of patients with metastatic renal cancer and is currently being trialled in other cancers. Sunitinib 81-90 vascular endothelial growth factor A Homo sapiens 40-44 21484496-2 2011 The first category, vascular endothelial growth factor (VEGF)-directed therapies, includes sunitinib, pazopanib, sorafenib and bevacizumab. Sunitinib 91-100 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. Sunitinib 91-100 vascular endothelial growth factor A Homo sapiens 56-60 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. Sunitinib 288-297 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. Sunitinib 288-297 vascular endothelial growth factor A Homo sapiens 232-236 21084271-0 2011 VEGF-PET imaging is a noninvasive biomarker showing differential changes in the tumor during sunitinib treatment. Sunitinib 93-102 vascular endothelial growth factor A Homo sapiens 0-4 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. Sunitinib 218-227 vascular endothelial growth factor A Homo sapiens 131-165 22050750-9 2011 Other small molecule inhibitors of VEGF tyrosine kinase activity (TKIs) such as sunitinib, vandetanib and sorafenib are being tested in MBC. Sunitinib 80-89 vascular endothelial growth factor A Homo sapiens 35-39 21717054-2 2011 Sunitinib is able to inhibit RTKs such as receptors for platelet-derived growth factor (PDGF-Ralpha and beta) and for vascular endothelial growth factor (VEGFRs). Sunitinib 0-9 vascular endothelial growth factor A Homo sapiens 118-152 21084271-2 2011 In this study, we evaluated the role of VEGF-PET as a biomarker of dynamic angiogenic changes in tumors following treatment with the kinase inhibitor sunitinib. Sunitinib 150-159 vascular endothelial growth factor A Homo sapiens 40-44 21084271-5 2011 In contrast to (18)F-FDG and (15)O-water PET, VEGF-PET demonstrated dynamic changes during sunitinib treatment within the tumor with a strong decline in signal in the tumor center and only minimal reduction in tumor rim, with a pronounced rebound after sunitinib discontinuation. Sunitinib 91-100 vascular endothelial growth factor A Homo sapiens 46-50 21980525-10 2011 In agreement, we observed that the binding of VEGFR2 to DNA requires VEGF activation, being blocked by Bevacizumab and Sunitinib, two anti-angiogenic agents that inhibit VEGFR2 activation. Sunitinib 119-128 vascular endothelial growth factor A Homo sapiens 46-50 20039326-6 2010 The addition of sunitinib to VEGF-stimulated NCI-N87 cells was associated with a reduction in MAPK phosphorylation (pMAPK) but not Akt phosphorylation (pAkt), whereas the addition of vandetanib was associated with reductions in both VEGF- and EGF-mediated VEGFR2 phosphorylation, pMAPK and pAkt. Sunitinib 16-25 vascular endothelial growth factor A Homo sapiens 29-33 20133148-3 2010 Sunitinib is an oral multitargeted inhibitor of the VEGF, platelet-derived growth factor (PDGF), and c-KIT, among others, tyrosine kinase receptors. Sunitinib 0-9 vascular endothelial growth factor A Homo sapiens 52-56 20142724-1 2010 OBJECTIVES: Sunitinib is an oral, multitargeted tyrosine kinase inhibitor of vascular endothelial growth factor and platelet-derived growth factor receptors with proven clinical benefit in patients with metastatic renal cell carcinoma (RCC). Sunitinib 12-21 vascular endothelial growth factor A Homo sapiens 77-111 21095547-4 2010 Recently, sunitinib demonstrating efficacy in pancreatic islet cell carcinomas has opened a new avenue for the treatment of NETs, and further trials shall be considered in NET types such as carcinoids, poorly differentiated neuroendocrine carcinomas, and several other endocrine tumors that depend on vascular endothelial growth factor (VEGF)/VEGF receptor for angiogenesis. Sunitinib 10-19 vascular endothelial growth factor A Homo sapiens 301-335 21095547-4 2010 Recently, sunitinib demonstrating efficacy in pancreatic islet cell carcinomas has opened a new avenue for the treatment of NETs, and further trials shall be considered in NET types such as carcinoids, poorly differentiated neuroendocrine carcinomas, and several other endocrine tumors that depend on vascular endothelial growth factor (VEGF)/VEGF receptor for angiogenesis. Sunitinib 10-19 vascular endothelial growth factor A Homo sapiens 337-341 21095547-4 2010 Recently, sunitinib demonstrating efficacy in pancreatic islet cell carcinomas has opened a new avenue for the treatment of NETs, and further trials shall be considered in NET types such as carcinoids, poorly differentiated neuroendocrine carcinomas, and several other endocrine tumors that depend on vascular endothelial growth factor (VEGF)/VEGF receptor for angiogenesis. Sunitinib 10-19 vascular endothelial growth factor A Homo sapiens 343-347 20471160-0 2010 mTOR inhibition by everolimus counteracts VEGF induction by sunitinib and improves anti-tumor activity against gastric cancer in vivo. Sunitinib 60-69 vascular endothelial growth factor A Homo sapiens 42-46 20471160-2 2010 We hypothesized that mTOR inhibition by everolimus counteracts VEGF induction by sunitinib resulting in an improved anti-tumor activity of sunitinib. Sunitinib 81-90 vascular endothelial growth factor A Homo sapiens 63-67 20471160-2 2010 We hypothesized that mTOR inhibition by everolimus counteracts VEGF induction by sunitinib resulting in an improved anti-tumor activity of sunitinib. Sunitinib 139-148 vascular endothelial growth factor A Homo sapiens 63-67 20471160-6 2010 In conclusion mTOR inhibition by everolimus counteracts VEGF induction by sunitinib and results in significant reduction of tumor burden and long-lasting tumor growth control. Sunitinib 74-83 vascular endothelial growth factor A Homo sapiens 56-60 20943646-9 2010 The vascular endothelial growth factor inhibitor sunitinib has demonstrated antitumor effects in pancreatic NETs. Sunitinib 49-58 vascular endothelial growth factor A Homo sapiens 4-38 20686367-10 2010 VEGF (10 ng/ml) caused a 42% increase in proliferation of E0771 cells, compared to the control (p < 0.01; n = 8), and there was a significant decrease in proliferation of E0771 cells treated with VEGF plus SU11248 (10 mumol/L) vs. the control (65%, p < 0.01). Sunitinib 209-216 vascular endothelial growth factor A Homo sapiens 0-4 20686367-11 2010 VEGF caused a 2-fold increase in the proliferation of HUVEC vs. the control (p < 0.01; n = 8), but its action was completely eradicated by SU11248. Sunitinib 142-149 vascular endothelial growth factor A Homo sapiens 0-4 20686367-15 2010 These findings support the hypothesis that the antitumor activity of SU11248 on breast cancer is possibly mediated by targeting the paracrine and autocrine effects of VEGF on breast cancer to suppress tumor angiogenesis, proliferation and migration. Sunitinib 69-76 vascular endothelial growth factor A Homo sapiens 167-171 20922699-7 2010 Inhibitors of vascular endothelial growth factor (VEGF), such as bevacizumab, sunitinib, and sorafenib, interfere with angiogenesis. Sunitinib 78-87 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. Sunitinib 78-87 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. Sunitinib 0-9 vascular endothelial growth factor A Homo sapiens 106-110 20039326-6 2010 The addition of sunitinib to VEGF-stimulated NCI-N87 cells was associated with a reduction in MAPK phosphorylation (pMAPK) but not Akt phosphorylation (pAkt), whereas the addition of vandetanib was associated with reductions in both VEGF- and EGF-mediated VEGFR2 phosphorylation, pMAPK and pAkt. Sunitinib 16-25 vascular endothelial growth factor A Homo sapiens 233-237 20629553-1 2010 BACKGROUND: Sunitinib malate (Sutent, Pfizer, Inc.; SU11248) is a selective, multitargeted inhibitor of receptor tyrosine kinases and has been shown to inhibit receptors for VEGF, PDGF, KIT, FLT3, and RET. Sunitinib 12-28 vascular endothelial growth factor A Homo sapiens 174-178 20629553-1 2010 BACKGROUND: Sunitinib malate (Sutent, Pfizer, Inc.; SU11248) is a selective, multitargeted inhibitor of receptor tyrosine kinases and has been shown to inhibit receptors for VEGF, PDGF, KIT, FLT3, and RET. Sunitinib 30-36 vascular endothelial growth factor A Homo sapiens 174-178 20629553-1 2010 BACKGROUND: Sunitinib malate (Sutent, Pfizer, Inc.; SU11248) is a selective, multitargeted inhibitor of receptor tyrosine kinases and has been shown to inhibit receptors for VEGF, PDGF, KIT, FLT3, and RET. Sunitinib 52-59 vascular endothelial growth factor A Homo sapiens 174-178 20601807-7 2010 Sunitinib, which targets VEGF-1, 2 and 3 and PDGF seems to be a well tolerated treatment for advanced tumors. Sunitinib 0-9 vascular endothelial growth factor A Homo sapiens 25-29 19547919-2 2010 We conducted a single-institution phase II trial of sunitinib, an oral inhibitor of the VEGF receptor, in patients with relapsed or refractory GCT. Sunitinib 52-61 vascular endothelial growth factor A Homo sapiens 88-92 20686603-12 2010 We show that VEGF triggered signal transduction via the MAPK pathway, which could be blocked by sunitinib. Sunitinib 96-105 vascular endothelial growth factor A Homo sapiens 13-17 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. Sunitinib 115-124 vascular endothelial growth factor A Homo sapiens 17-21 20187785-1 2010 BACKGROUND: Sunitinib is a small molecule that inhibits receptor tyrosine kinases, including the vascular endothelial growth factor receptors, and exhibits antiangiogenic and antitumor activity. Sunitinib 12-21 vascular endothelial growth factor A Homo sapiens 97-131 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. Sunitinib 83-92 vascular endothelial growth factor A Homo sapiens 62-66 20502715-0 2010 Soluble isoforms of vascular endothelial growth factor are predictors of response to sunitinib in metastatic renal cell carcinomas. Sunitinib 85-94 vascular endothelial growth factor A Homo sapiens 20-54 20502715-8 2010 Among transcripts analyzed, only the levels of vascular endothelial growth factor (VEGF) soluble isoforms (VEGF(121) and VEGF(165)) were associated with the response to sunitinib (P = 0.04 for both). Sunitinib 169-178 vascular endothelial growth factor A Homo sapiens 47-81 20502715-8 2010 Among transcripts analyzed, only the levels of vascular endothelial growth factor (VEGF) soluble isoforms (VEGF(121) and VEGF(165)) were associated with the response to sunitinib (P = 0.04 for both). Sunitinib 169-178 vascular endothelial growth factor A Homo sapiens 83-87 20502715-8 2010 Among transcripts analyzed, only the levels of vascular endothelial growth factor (VEGF) soluble isoforms (VEGF(121) and VEGF(165)) were associated with the response to sunitinib (P = 0.04 for both). Sunitinib 169-178 vascular endothelial growth factor A Homo sapiens 107-111 20502715-8 2010 Among transcripts analyzed, only the levels of vascular endothelial growth factor (VEGF) soluble isoforms (VEGF(121) and VEGF(165)) were associated with the response to sunitinib (P = 0.04 for both). Sunitinib 169-178 vascular endothelial growth factor A Homo sapiens 107-111 20147887-0 2010 Predictive value of baseline serum vascular endothelial growth factor and neutrophil gelatinase-associated lipocalin in advanced kidney cancer patients receiving sunitinib. Sunitinib 162-171 vascular endothelial growth factor A Homo sapiens 35-69 20147887-7 2010 Our study shows that serum levels of VEGF and NGAL are significant predictors of progression-free survival in patients with renal cell carcinoma treated with sunitinib. Sunitinib 158-167 vascular endothelial growth factor A Homo sapiens 37-41 20658715-2 2010 Vascular endothelial growth factor (VEGF) pathway is the principle target for drugs like sunitinib, sorafenib and bevacizumab. Sunitinib 89-98 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. Sunitinib 89-98 vascular endothelial growth factor A Homo sapiens 36-40 19740535-2 2010 Sunitinib malate is an oral, multi-targeted tyrosine kinase inhibitor that inhibits receptors for VEGF, c-Kit and platelet-derived growth factor. Sunitinib 0-16 vascular endothelial growth factor A Homo sapiens 98-102 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. Sunitinib 42-51 vascular endothelial growth factor A Homo sapiens 103-137 19911111-1 2009 Sunitinib demonstrating efficacy in pancreatic islet cell carcinomas will pave the way for further trials in other neuroendocrine tumor types such as carcinoid, poorly differentiated neuroendocrine disease, and several other endocrine tumors that are dependent on VEGF/VEGFR for angiogenesis. Sunitinib 0-9 vascular endothelial growth factor A Homo sapiens 264-268 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. Sunitinib 164-173 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. Sunitinib 296-305 vascular endothelial growth factor A Homo sapiens 210-214 20102396-9 2010 In vitro, addition of sunitinib prevented the release of endocan in human umbilical vascular endothelial cells when induced by vascular endothelial growth factor. Sunitinib 22-31 vascular endothelial growth factor A Homo sapiens 127-161 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. Sunitinib 88-97 vascular endothelial growth factor A Homo sapiens 34-38 20949248-2 2010 Sunitinib is able to inhibit RTKs such as receptors for platelet-derived growth factor (PDGF-R alpha and beta) and for vascular endothelial growth factor (VEGFRs). Sunitinib 0-9 vascular endothelial growth factor A Homo sapiens 119-153 19940466-5 2010 Sunitinib, a small molecule blocking intracellular VEGF, KIT, Flt3 and PDGF receptors, which regulate angiogenesis and cell growth, is approved for the treatment of advanced renal cell cancer (RCC) and malignant gastrointestinal stromal tumor. Sunitinib 0-9 vascular endothelial growth factor A Homo sapiens 51-55 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. Sunitinib 73-82 vascular endothelial growth factor A Homo sapiens 53-57 19318229-5 2009 ZD6474 and ZD1839 inhibited EGF-induced phosphorylation of EGFR, AKT and ERK, whereas VEGF-induced phosphorylation of VEGFR2 was completely inhibited with 0.1 microM SU11248. Sunitinib 166-173 vascular endothelial growth factor A Homo sapiens 86-90 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. Sunitinib 142-151 vascular endothelial growth factor A Homo sapiens 99-103 19773375-1 2009 PURPOSE: Bevacizumab is an antibody against vascular endothelial growth factor; sunitinib is an inhibitor of vascular endothelial growth factor and related receptors. Sunitinib 80-89 vascular endothelial growth factor A Homo sapiens 109-143 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. Sunitinib 54-63 vascular endothelial growth factor A Homo sapiens 104-108 21789110-3 2009 Bevacizumab is directed against the vascular endothelial growth factor (VEGF), a key mediator of angiogenesis, whilst sorafenib and sunitinib inhibit a number of targets including the VEGF and platelet-derived growth factor (PDGFR) receptor tyrosine kinases. Sunitinib 132-141 vascular endothelial growth factor A Homo sapiens 184-188 18534874-1 2009 PURPOSE: Sunitinib malate (Pfizer, Inc.) is a multitargeted kinase inhibitor that inhibits vascular endothelial growth factor (VEGF) receptor (R)-1, 2 and 3, platelet-derived growth factor receptors (PDGFR)-alpha and beta, Flt3, RET, and Kit. Sunitinib 9-25 vascular endothelial growth factor A Homo sapiens 127-131 19224847-1 2009 PURPOSE: Both bevacizumab and sunitinib target the vascular endothelial growth factor pathway and demonstrate activity against advanced renal cell carcinoma (RCC). Sunitinib 30-39 vascular endothelial growth factor A Homo sapiens 51-85 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. Sunitinib 112-121 vascular endothelial growth factor A Homo sapiens 196-200 19336014-2 2009 Dissection of the molecular pathways that regulate proliferation, apoptosis, and angiogenesis has led to the development of targeted therapies such as the receptor tyrosine kinase inhibitors sunitinib and sorafenib, the anti-vascular endothelial growth factor antibody bevacizumab, and a class of rapamycin analogues including everolimus and temsirolimus. Sunitinib 191-200 vascular endothelial growth factor A Homo sapiens 225-259 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. Sunitinib 0-16 vascular endothelial growth factor A Homo sapiens 181-215 19402073-3 2009 Approaches to bind circulating VEGF protein (eg, bevacizumab) and small molecule inhibitors of the receptor on which the VEGF ligand binds (eg, sunitinib, sorafenib, axitinib, and pazopanib) have been tested. Sunitinib 144-153 vascular endothelial growth factor A Homo sapiens 121-125 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. Sunitinib 27-36 vascular endothelial growth factor A Homo sapiens 44-48 19017755-6 2009 Patient was treated with sunitinib, a potent tyrosine kinase inhibitor of vascular endothelial growth factor, platelet-derived growth factor, RET, c-KIT, and FLT-3 receptors. Sunitinib 25-34 vascular endothelial growth factor A Homo sapiens 74-108 19891126-5 2008 This review will summarize the major clinical trials and practical recommendations for the most studied VEGF inhibitors, including sunitinib, sorafenib, and bevacizumab; introduce novel VEGF inhibitor agents; outline side effects and toxicities; and discuss sequential and combination therapy with these agents. Sunitinib 131-140 vascular endothelial growth factor A Homo sapiens 104-108 19096396-2 2009 In 2007, a pivotal phase III trial randomly allocated 750 patients with advanced renal cell carcinoma to receive either the VEGF-receptor tyrosine kinase inhibitor sunitinib or interferon alpha, and showed that sunitinib led to improved response rates, progression-free and overall survival. Sunitinib 211-220 vascular endothelial growth factor A Homo sapiens 124-128 19054798-0 2009 Thrombotic microangiopathy secondary to VEGF pathway inhibition by sunitinib. Sunitinib 67-76 vascular endothelial growth factor A Homo sapiens 40-44 19054798-3 2009 It was shown recently that sunitinib, a small molecule inhibiting several tyrosine kinase receptors, including VEGF receptors, can also induce proteinuria, hypertension and biological features of TMA. Sunitinib 27-36 vascular endothelial growth factor A Homo sapiens 111-115 19105714-1 2009 Sunitinib malate is an oral, multitargeted receptor tyrosine kinase inhibitor of VEGF receptors 1, 2 and 3; PDGF receptors alpha and beta, and other receptor tyrosine kinases implicated in tumor growth, angiogenesis and metastasis. Sunitinib 0-16 vascular endothelial growth factor A Homo sapiens 81-85 19096396-2 2009 In 2007, a pivotal phase III trial randomly allocated 750 patients with advanced renal cell carcinoma to receive either the VEGF-receptor tyrosine kinase inhibitor sunitinib or interferon alpha, and showed that sunitinib led to improved response rates, progression-free and overall survival. Sunitinib 164-173 vascular endothelial growth factor A Homo sapiens 124-128 18472378-2 2008 Among them, the major are those targeting the VEGF pathway, including anti-VEGF antibodies (bevacizumab) and VEGF receptor tyrosine kinase inhibitors (vatalanib, sorafenib, sunitinib...). Sunitinib 173-182 vascular endothelial growth factor A Homo sapiens 46-50 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. Sunitinib 0-16 vascular endothelial growth factor A Homo sapiens 181-185 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. Sunitinib 72-81 vascular endothelial growth factor A Homo sapiens 33-37 19075590-4 2008 Both sunitinib and sorafenib target VEGF and PDGF receptor tyrosine kinases while bevacizumab is a monoclonal antibody to VEGF. Sunitinib 5-14 vascular endothelial growth factor A Homo sapiens 36-40 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). Sunitinib 12-21 vascular endothelial growth factor A Homo sapiens 73-107 18669461-11 2008 CONCLUSION: Sunitinib has substantial antitumor activity in patients with bevacizumab-refractory mRCC and modulates circulating VEGF pathway biomarkers. Sunitinib 12-21 vascular endothelial growth factor A Homo sapiens 128-132 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. Sunitinib 188-197 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. Sunitinib 199-205 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). Sunitinib 180-189 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. Sunitinib 66-75 vascular endothelial growth factor A Homo sapiens 50-54 18235126-2 2008 We evaluated the clinical activity and tolerability of sunitinib malate (SU11248), an oral, multitargeted tyrosine kinase inhibitor that blocks the activity of receptors for VEGF and PDGF, as well as related tyrosine kinases in patients with previously treated, advanced NSCLC. Sunitinib 55-71 vascular endothelial growth factor A Homo sapiens 174-178 18235126-2 2008 We evaluated the clinical activity and tolerability of sunitinib malate (SU11248), an oral, multitargeted tyrosine kinase inhibitor that blocks the activity of receptors for VEGF and PDGF, as well as related tyrosine kinases in patients with previously treated, advanced NSCLC. Sunitinib 73-80 vascular endothelial growth factor A Homo sapiens 174-178 18192256-2 2008 SUMMARY: Sunitinib malate is a potent inhibitor of vascular endothelial growth factor (VEGF) receptors, FMS-like tyrosine kinase 3 (FLT3), c-KIT, and platelet-derived growth factor (PDGF), which give the drug its direct antitumor and antiangiogenic properties. Sunitinib 9-25 vascular endothelial growth factor A Homo sapiens 51-85 18192256-2 2008 SUMMARY: Sunitinib malate is a potent inhibitor of vascular endothelial growth factor (VEGF) receptors, FMS-like tyrosine kinase 3 (FLT3), c-KIT, and platelet-derived growth factor (PDGF), which give the drug its direct antitumor and antiangiogenic properties. Sunitinib 9-25 vascular endothelial growth factor A Homo sapiens 87-91 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. Sunitinib 76-85 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. Sunitinib 87-93 vascular endothelial growth factor A Homo sapiens 127-161 18272027-1 2007 Sunitinib is a tyrosine kinase inhibitor with activity against vascular endothelial growth factor (VEGF) receptor and platelet-derived growth factor receptor recently approved by the FDA for the treatment of advanced renal cell carcinoma (RCC). Sunitinib 0-9 vascular endothelial growth factor A Homo sapiens 99-103 17657252-5 2007 Sunitinib, sorafenib and axitinib are kinase inhibitors that inhibit the VEGF, platelet-derived growth factor and c-kit receptor tyrosine kinases. Sunitinib 0-9 vascular endothelial growth factor A Homo sapiens 73-77 17710208-2 2007 Because angiogenesis is necessary for the growth and metastasis of solid tumours, and VEGF is believed to have a pivotal role in that process, SUNITINIB treatment may have broad-spectrum clinical utility. Sunitinib 143-152 vascular endothelial growth factor A Homo sapiens 86-90 17605814-0 2007 Circulating protein biomarkers of pharmacodynamic activity of sunitinib in patients with metastatic renal cell carcinoma: modulation of VEGF and VEGF-related proteins. Sunitinib 62-71 vascular endothelial growth factor A Homo sapiens 136-140 17605814-0 2007 Circulating protein biomarkers of pharmacodynamic activity of sunitinib in patients with metastatic renal cell carcinoma: modulation of VEGF and VEGF-related proteins. Sunitinib 62-71 vascular endothelial growth factor A Homo sapiens 145-149 17605814-9 2007 CONCLUSION: Sunitinib treatment in advanced RCC patients leads to modulation of plasma levels of circulating proteins involved in VEGF signaling, including soluble forms of two VEGF receptors. Sunitinib 12-21 vascular endothelial growth factor A Homo sapiens 130-134 17605814-9 2007 CONCLUSION: Sunitinib treatment in advanced RCC patients leads to modulation of plasma levels of circulating proteins involved in VEGF signaling, including soluble forms of two VEGF receptors. Sunitinib 12-21 vascular endothelial growth factor A Homo sapiens 177-181 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. Sunitinib 243-252 vascular endothelial growth factor A Homo sapiens 27-31 17588358-2 2007 Sunitinib is a tyrosine kinase inhibitor with a wide range of kinase inhibition, including KIT, platelet-derived growth factor receptor (PDGFR), vascular endothelial growth factor (VEGF), and FLT3. Sunitinib 0-9 vascular endothelial growth factor A Homo sapiens 145-179 17588358-2 2007 Sunitinib is a tyrosine kinase inhibitor with a wide range of kinase inhibition, including KIT, platelet-derived growth factor receptor (PDGFR), vascular endothelial growth factor (VEGF), and FLT3. Sunitinib 0-9 vascular endothelial growth factor A Homo sapiens 181-185 17367763-0 2007 Sunitinib: a VEGF and PDGF receptor protein kinase and angiogenesis inhibitor. Sunitinib 0-9 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. Sunitinib 150-159 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. Sunitinib 150-159 vascular endothelial growth factor A Homo sapiens 115-119 17202116-1 2007 Sunitinib is an inhibitor of the vascular endothelial growth factor and platelet-derived growth factor receptors, and it has antitumor activity in metastatic renal cell carcinoma and gastrointestinal stromal tumors. Sunitinib 0-9 vascular endothelial growth factor A Homo sapiens 33-67 17255305-5 2007 In contrast, two multitargeted receptor tyrosine kinase inhibitors that target both VEGF and PDGF receptors (sunitinib and AG013736) have shown > or =40% objective responses with clinically important duration. Sunitinib 109-118 vascular endothelial growth factor A Homo sapiens 84-88 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. Sunitinib 49-58 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. Sunitinib 0-9 vascular endothelial growth factor A Homo sapiens 123-127 16974118-8 2006 This opens interesting new treatment strategies including blockade of VEGF with the monoclonal antibody bevacizumab (Avastin) and inhibition of VEGF receptor tyrosine kinases with small oral molecules such as sunitinib (SU11248, Sutent) or PTK787. Sunitinib 209-218 vascular endothelial growth factor A Homo sapiens 144-148 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. Sunitinib 0-9 vascular endothelial growth factor A Homo sapiens 85-119 12538485-0 2003 In vivo antitumor activity of SU11248, a novel tyrosine kinase inhibitor targeting vascular endothelial growth factor and platelet-derived growth factor receptors: determination of a pharmacokinetic/pharmacodynamic relationship. Sunitinib 30-37 vascular endothelial growth factor A Homo sapiens 83-117 16330672-2 2006 SU11248 (sunitinib malate), a small molecule inhibitor with high binding affinity for VEGF and PDGF receptors, was tested for clinical activity in patients with metastatic RCC. Sunitinib 0-7 vascular endothelial growth factor A Homo sapiens 86-90 16330672-9 2006 CONCLUSION: SU11248, a multitargeted receptor tyrosine kinase inhibitor of VEGF and PDGF receptors, demonstrates antitumor activity in metastatic RCC as second-line therapy, a setting where no effective systemic therapy is presently recognized. Sunitinib 12-19 vascular endothelial growth factor A Homo sapiens 75-79 15609077-2 2004 To determine whether the vascular endothelial growth factor (VEGF) receptor is a molecular target to prevent metastatic disease, we utilized a non-specific inhibitor of the VEGF receptor, SU11248. Sunitinib 188-195 vascular endothelial growth factor A Homo sapiens 61-65 15609077-2 2004 To determine whether the vascular endothelial growth factor (VEGF) receptor is a molecular target to prevent metastatic disease, we utilized a non-specific inhibitor of the VEGF receptor, SU11248. Sunitinib 188-195 vascular endothelial growth factor A Homo sapiens 173-177 16685460-3 2006 Bevacizumab (Avastin), Sunitinib (Sutent) and Sorafenib (Nexavar) are anti-cancer drugs targeted to VEGF signaling pathway. Sunitinib 23-32 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. Sunitinib 34-40 vascular endothelial growth factor A Homo sapiens 100-104 16731761-2 2006 SU11248, a small-molecule inhibitor targeting class III/V receptor tyrosine kinases, including the platelet-derived growth factor (PDGF) and vascular endothelial growth factor (VEGF) receptors, KIT and FLT3, exhibits direct effects on cancer cells as well as antiangiogenic activity. Sunitinib 0-7 vascular endothelial growth factor A Homo sapiens 141-175 16731761-5 2006 To elucidate the specific contributions of inhibition of PDGF and VEGF receptors to the in vivo efficacy of SU11248, we employed two selective inhibitors, SU10944 (VEGF receptor inhibitor) and Gleevec (PDGF receptor inhibitor). Sunitinib 108-115 vascular endothelial growth factor A Homo sapiens 66-70 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. Sunitinib 93-109 vascular endothelial growth factor A Homo sapiens 147-151 16425985-2 2005 SU11248 and AG013736 are small-molecule inhibitors of the tyrosine kinase portion of the VEGF and PDGF receptors. Sunitinib 0-7 vascular endothelial growth factor A Homo sapiens 89-93 16185167-4 2005 Results using small-molecule inhibitors of VEGF, FLT3, KIT and platelet-derived growth factor receptor tyrosine kinases, such as sunitinib, show a 40% objective response rate. Sunitinib 129-138 vascular endothelial growth factor A Homo sapiens 43-47 12531805-8 2003 In addition, SU11248 inhibits FLT3-induced VEGF production. Sunitinib 13-20 vascular endothelial growth factor A Homo sapiens 43-47 12538485-3 2003 SU11248, a novel small molecule receptor tyrosine kinase inhibitor with direct antitumor as well as antiangiogenic activity via targeting the vascular endothelial growth factor (VEGF), platelet-derived growth factor (PDGF), KIT, and FLT3 receptor tyrosine kinases, was used as the pharmacological agent in these studies. Sunitinib 0-7 vascular endothelial growth factor A Homo sapiens 142-176 12538485-3 2003 SU11248, a novel small molecule receptor tyrosine kinase inhibitor with direct antitumor as well as antiangiogenic activity via targeting the vascular endothelial growth factor (VEGF), platelet-derived growth factor (PDGF), KIT, and FLT3 receptor tyrosine kinases, was used as the pharmacological agent in these studies. Sunitinib 0-7 vascular endothelial growth factor A Homo sapiens 178-182 12538485-6 2003 In target modulation studies in vivo, SU11248 selectively inhibited Flk-1/KDR (VEGF receptor 2) and PDGF receptor beta phosphorylation (in a time- and dose-dependent manner) when plasma concentrations of inhibitor reached or exceeded 50-100 ng/ml. Sunitinib 38-45 vascular endothelial growth factor A Homo sapiens 79-83 14988747-8 2003 Although very preliminary, a phase I trial found tumor regressions that were caused by an oral VEGF receptor tyrosine kinase inhibitor, SU11248. Sunitinib 136-143 vascular endothelial growth factor A Homo sapiens 95-99