PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 17327610-3 2007 Sunitinib inhibits other tyrosine kinases including, KIT, FLT3, colony-stimulating factor 1 (CSF-1), and RET, which are involved in a number of malignancies including small-cell lung cancer, GI stromal tumors (GISTs), breast cancer, acute myelogenous leukemia, multiple endocrine neoplasia types 2A and 2B, and familial medullary thyroid carcinoma. Sunitinib 0-9 ret proto-oncogene Homo sapiens 105-108 16849418-0 2006 An orally administered multitarget tyrosine kinase inhibitor, SU11248, is a novel potent inhibitor of thyroid oncogenic RET/papillary thyroid cancer kinases. Sunitinib 62-69 ret proto-oncogene Homo sapiens 120-123 16849418-8 2006 RET/PTC-mediated Y705 phosphorylation of STAT3 was inhibited by addition of SU11248, and the inhibitory effects of SU11248 on the tyrosine phosphorylation and transcriptional activation of STAT3 were very closely correlated with decreased autophosphorylation of RET/PTC. Sunitinib 76-83 ret proto-oncogene Homo sapiens 0-3 16849418-8 2006 RET/PTC-mediated Y705 phosphorylation of STAT3 was inhibited by addition of SU11248, and the inhibitory effects of SU11248 on the tyrosine phosphorylation and transcriptional activation of STAT3 were very closely correlated with decreased autophosphorylation of RET/PTC. Sunitinib 76-83 ret proto-oncogene Homo sapiens 4-7 16849418-8 2006 RET/PTC-mediated Y705 phosphorylation of STAT3 was inhibited by addition of SU11248, and the inhibitory effects of SU11248 on the tyrosine phosphorylation and transcriptional activation of STAT3 were very closely correlated with decreased autophosphorylation of RET/PTC. Sunitinib 115-122 ret proto-oncogene Homo sapiens 0-3 16849418-8 2006 RET/PTC-mediated Y705 phosphorylation of STAT3 was inhibited by addition of SU11248, and the inhibitory effects of SU11248 on the tyrosine phosphorylation and transcriptional activation of STAT3 were very closely correlated with decreased autophosphorylation of RET/PTC. Sunitinib 115-122 ret proto-oncogene Homo sapiens 4-7 16849418-8 2006 RET/PTC-mediated Y705 phosphorylation of STAT3 was inhibited by addition of SU11248, and the inhibitory effects of SU11248 on the tyrosine phosphorylation and transcriptional activation of STAT3 were very closely correlated with decreased autophosphorylation of RET/PTC. Sunitinib 115-122 ret proto-oncogene Homo sapiens 262-265 16849418-8 2006 RET/PTC-mediated Y705 phosphorylation of STAT3 was inhibited by addition of SU11248, and the inhibitory effects of SU11248 on the tyrosine phosphorylation and transcriptional activation of STAT3 were very closely correlated with decreased autophosphorylation of RET/PTC. Sunitinib 115-122 ret proto-oncogene Homo sapiens 266-269 16849418-9 2006 SU11248 caused a complete morphological reversion of transformed NIH-RET/PTC3 cells and inhibited the growth of TPC-1 cells that have an endogenous RET/PTC1. Sunitinib 0-7 ret proto-oncogene Homo sapiens 69-72 16849418-9 2006 SU11248 caused a complete morphological reversion of transformed NIH-RET/PTC3 cells and inhibited the growth of TPC-1 cells that have an endogenous RET/PTC1. Sunitinib 0-7 ret proto-oncogene Homo sapiens 148-151 16849418-10 2006 CONCLUSION: SU11248 is a highly effective tyrosine kinase inhibitor of the RET/PTC oncogenic kinase. Sunitinib 12-19 ret proto-oncogene Homo sapiens 75-78 16849418-10 2006 CONCLUSION: SU11248 is a highly effective tyrosine kinase inhibitor of the RET/PTC oncogenic kinase. Sunitinib 12-19 ret proto-oncogene Homo sapiens 79-82 16849418-3 2006 OBJECTIVE: The objective of the study was to evaluate the efficacies of the recently developed kinase inhibitors SU11248, SU5416, and SU6668 in inhibition of RET/PTC. Sunitinib 113-120 ret proto-oncogene Homo sapiens 158-161 16849418-3 2006 OBJECTIVE: The objective of the study was to evaluate the efficacies of the recently developed kinase inhibitors SU11248, SU5416, and SU6668 in inhibition of RET/PTC. Sunitinib 113-120 ret proto-oncogene Homo sapiens 162-165 16849418-4 2006 DESIGN: SU11248, SU5416, and SU6668 were synthesized, and their inhibitory potencies were evaluated using an in vitro RET/PTC kinase assay. Sunitinib 8-15 ret proto-oncogene Homo sapiens 122-125 16849418-6 2006 RESULTS: An in vitro kinase assay revealed that SU5416, SU6668, and SU11248 inhibited phosphorylation of the synthetic tyrosine kinase substrate peptide E4Y by RET/PTC3 in a dose-dependent manner with IC(50) of approximately 944 nm for SU5416, 562 nm for SU6668, and 224 nm for SU11248. Sunitinib 68-75 ret proto-oncogene Homo sapiens 160-163 16849418-6 2006 RESULTS: An in vitro kinase assay revealed that SU5416, SU6668, and SU11248 inhibited phosphorylation of the synthetic tyrosine kinase substrate peptide E4Y by RET/PTC3 in a dose-dependent manner with IC(50) of approximately 944 nm for SU5416, 562 nm for SU6668, and 224 nm for SU11248. Sunitinib 278-285 ret proto-oncogene Homo sapiens 160-163 16849418-7 2006 Thus, SU11248 effectively inhibits the kinase activity of RET/PTC3. Sunitinib 6-13 ret proto-oncogene Homo sapiens 58-61 15609077-0 2004 The receptor tyrosine kinase inhibitor SU11248 impedes endothelial cell migration, tubule formation, and blood vessel formation in vivo, but has little effect on existing tumor vessels. Sunitinib 39-46 ret proto-oncogene Homo sapiens 4-28 32814829-2 2020 Receptor tyrosine kinase (RTK) inhibitors such as sunitinib have been demonstrated to target tumorigenic signaling pathways, delay tumor progression, and improve patient prognosis in metastatic renal cell carcinoma (mRCC). Sunitinib 50-59 ret proto-oncogene Homo sapiens 0-24 35500680-2 2022 Systemic chemotherapy such as cisplatin and multi-targeted receptor tyrosine kinase inhibitors, including sunitinib, has marginal activity and frequent toxicity. Sunitinib 106-115 ret proto-oncogene Homo sapiens 59-83 35358627-1 2022 The efficacy/safety of combining palbociclib (a CDK4/6 inhibitor) and sunitinib (a multi-targeted receptor tyrosine kinase inhibitor) was evaluated, using patient-derived xenograft (PDX) models. Sunitinib 70-79 ret proto-oncogene Homo sapiens 98-122 32814829-2 2020 Receptor tyrosine kinase (RTK) inhibitors such as sunitinib have been demonstrated to target tumorigenic signaling pathways, delay tumor progression, and improve patient prognosis in metastatic renal cell carcinoma (mRCC). Sunitinib 50-59 ret proto-oncogene Homo sapiens 26-29 31025080-1 2019 Sunitinib (SNT) is a multi-targeted receptor tyrosine kinase inhibitor that has been approved by the FDA for cancer therapy. Sunitinib 0-9 ret proto-oncogene Homo sapiens 36-60 32578660-3 2020 Herein, the multi-targeted receptor tyrosine kinase (RTK) inhibitor sunitinib (Sun) and photodynamic therapy (PDT) drug chlorin e6 (Ce6) were locally delivered to the postoperative tumor site via a zwitterionic hydrogel. Sunitinib 68-77 ret proto-oncogene Homo sapiens 27-51 32578660-3 2020 Herein, the multi-targeted receptor tyrosine kinase (RTK) inhibitor sunitinib (Sun) and photodynamic therapy (PDT) drug chlorin e6 (Ce6) were locally delivered to the postoperative tumor site via a zwitterionic hydrogel. Sunitinib 68-77 ret proto-oncogene Homo sapiens 53-56 31025080-1 2019 Sunitinib (SNT) is a multi-targeted receptor tyrosine kinase inhibitor that has been approved by the FDA for cancer therapy. Sunitinib 11-14 ret proto-oncogene Homo sapiens 36-60 28990511-1 2019 BACKGROUND: Sunitinib (SU11248) is an oral multi-target tyrosine kinase inhibitor (TKI) with low molecular weight, that inhibits platelet-derived growth factor receptors (PDGF-Rs) and vascular endothelial growth factor receptors (VEGFRs), c-KIT, fms-related tyrosine kinase 3 (FLT3) and RET. Sunitinib 12-21 ret proto-oncogene Homo sapiens 287-290 28990511-1 2019 BACKGROUND: Sunitinib (SU11248) is an oral multi-target tyrosine kinase inhibitor (TKI) with low molecular weight, that inhibits platelet-derived growth factor receptors (PDGF-Rs) and vascular endothelial growth factor receptors (VEGFRs), c-KIT, fms-related tyrosine kinase 3 (FLT3) and RET. Sunitinib 23-30 ret proto-oncogene Homo sapiens 287-290 28990511-5 2019 RESULTS: In vitro studies showed that sunitinib targeted the cytosolic MEK/ERK and SAPK/JNK pathways in the RET/PTC1 cell inhibiting cell proliferation and causing stimulation of sodium/iodide symporter (NIS) gene expression in RET/PTC1 cells. Sunitinib 38-47 ret proto-oncogene Homo sapiens 108-111 28990511-5 2019 RESULTS: In vitro studies showed that sunitinib targeted the cytosolic MEK/ERK and SAPK/JNK pathways in the RET/PTC1 cell inhibiting cell proliferation and causing stimulation of sodium/iodide symporter (NIS) gene expression in RET/PTC1 cells. Sunitinib 38-47 ret proto-oncogene Homo sapiens 228-231 25971960-0 2015 Receptor Tyrosine Kinase Expression Predicts Response to Sunitinib in Breast Cancer. Sunitinib 57-66 ret proto-oncogene Homo sapiens 0-24 28736633-3 2017 Through a number of clinical trials, the mTOR inhibitor everolimus and the receptor tyrosine kinase (RTK) inhibitor sunitinib were recently approved for NETs. Sunitinib 116-125 ret proto-oncogene Homo sapiens 75-99 28736633-3 2017 Through a number of clinical trials, the mTOR inhibitor everolimus and the receptor tyrosine kinase (RTK) inhibitor sunitinib were recently approved for NETs. Sunitinib 116-125 ret proto-oncogene Homo sapiens 101-104 28105557-3 2017 Although no treatments are currently available to manage HAND, we have previously shown that sunitinib, an anticancer drug that blocks receptor tyrosine-kinase and cyclin kinase pathways, might be of interest. Sunitinib 93-102 ret proto-oncogene Homo sapiens 135-159 27149458-6 2016 Gene mutations in the genes encoding EGFR, FGFR2, KDR, and RET were discovered in the patient"s tumor tissue by whole exome sequencing and the patient was treated with a combination of the targeted drugs cetuximab and sunitinib. Sunitinib 218-227 ret proto-oncogene Homo sapiens 59-62 28693255-1 2017 Sunitinib (SU) is a small molecule that inhibits the receptor tyrosine kinase (RTK) signaling pathway, and has been clinically used to treat advanced renal cell carcinoma (RCC). Sunitinib 0-9 ret proto-oncogene Homo sapiens 53-77 28693255-1 2017 Sunitinib (SU) is a small molecule that inhibits the receptor tyrosine kinase (RTK) signaling pathway, and has been clinically used to treat advanced renal cell carcinoma (RCC). Sunitinib 0-9 ret proto-oncogene Homo sapiens 79-82 28693255-1 2017 Sunitinib (SU) is a small molecule that inhibits the receptor tyrosine kinase (RTK) signaling pathway, and has been clinically used to treat advanced renal cell carcinoma (RCC). Sunitinib 11-13 ret proto-oncogene Homo sapiens 53-77 28693255-1 2017 Sunitinib (SU) is a small molecule that inhibits the receptor tyrosine kinase (RTK) signaling pathway, and has been clinically used to treat advanced renal cell carcinoma (RCC). Sunitinib 11-13 ret proto-oncogene Homo sapiens 79-82 24424564-1 2014 Sunitinib is a tyrosine kinase inhibitor with direct anti-tumor and anti-angiogenesis activity targeting VEGFR 1-2, PDGFR alpha-beta, c-kit, bFGF, (CSF-1), FLT3 and RET. Sunitinib 0-9 ret proto-oncogene Homo sapiens 165-168 26003083-5 2015 Increased Cx43 expression in an MM cell line (H28) improved the ability of SU to inhibit receptor tyrosine kinase (RTK) signaling. Sunitinib 75-77 ret proto-oncogene Homo sapiens 89-113 26003083-5 2015 Increased Cx43 expression in an MM cell line (H28) improved the ability of SU to inhibit receptor tyrosine kinase (RTK) signaling. Sunitinib 75-77 ret proto-oncogene Homo sapiens 115-118 25637219-3 2015 We recently identified the RTK AXL as a putative target for the pan-RTK inhibitors cediranib and sunitinib, which are under clinical trials for glioblastoma patients. Sunitinib 97-106 ret proto-oncogene Homo sapiens 27-30 25637219-3 2015 We recently identified the RTK AXL as a putative target for the pan-RTK inhibitors cediranib and sunitinib, which are under clinical trials for glioblastoma patients. Sunitinib 97-106 ret proto-oncogene Homo sapiens 68-71 25376776-7 2015 In the presence of VEGF stimulation, the ROCK inhibitor suppressed stretch-induced sprout alignment but did not affect stretch-induced sprout density; in contrast, the receptor tyrosine kinase (RTK) inhibitor sunitinib had no effect on stretch-induced alignment but trended toward suppressed stretch-induced sprout density. Sunitinib 209-218 ret proto-oncogene Homo sapiens 194-197 26291023-0 2015 Rapid Response to Sunitinib in a Patient with Lung Adenocarcinoma Harboring KIF5B-RET Fusion Gene. Sunitinib 18-27 ret proto-oncogene Homo sapiens 82-85 24045439-8 2014 Similarly, sunitinib, a small-molecule inhibitor of RET, blocked GDNF-mediated activation of ERK and AKT. Sunitinib 11-20 ret proto-oncogene Homo sapiens 52-55 25085632-0 2014 Next generation sequencing analysis of platinum refractory advanced germ cell tumor sensitive to Sunitinib (Sutent ) a VEGFR2/PDGFRbeta/c-kit/ FLT3/RET/CSF1R inhibitor in a phase II trial. Sunitinib 97-106 ret proto-oncogene Homo sapiens 148-151 25085632-9 2014 Next generation sequencing to understand this patient"s response to sunitinib revealed RET amplification, EGFR and KRAS amplification as relevant aberrations. Sunitinib 68-77 ret proto-oncogene Homo sapiens 87-90 25085632-12 2014 Next generation sequencing of this "exceptional responder" identified the first reported case of a RET amplification as a potential basis of sensitivity to sunitinib (VEGFR2/PDGFRbeta/c-kit/ FLT3/RET/CSF1R inhibitor) in a patient with refractory germ cell tumor. Sunitinib 156-165 ret proto-oncogene Homo sapiens 99-102 25085632-12 2014 Next generation sequencing of this "exceptional responder" identified the first reported case of a RET amplification as a potential basis of sensitivity to sunitinib (VEGFR2/PDGFRbeta/c-kit/ FLT3/RET/CSF1R inhibitor) in a patient with refractory germ cell tumor. Sunitinib 156-165 ret proto-oncogene Homo sapiens 196-199 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 ret proto-oncogene Homo sapiens 47-50 24703573-13 2014 Among putative sunitinib targets, only RET was expressed and activated in analysed samples. Sunitinib 15-24 ret proto-oncogene Homo sapiens 39-42 24045439-9 2014 Inhibition of RET either by gene knockdown or by treatment with sunitinib or vandetanib reduced RET-dependent growth of luminal breast cancer cells. Sunitinib 64-73 ret proto-oncogene Homo sapiens 14-17 24045439-9 2014 Inhibition of RET either by gene knockdown or by treatment with sunitinib or vandetanib reduced RET-dependent growth of luminal breast cancer cells. Sunitinib 64-73 ret proto-oncogene Homo sapiens 96-99 24045439-11 2014 Parallel experiments using treatment with tamoxifen and sunitinib confirmed the increased effectiveness of dual inhibition of the ER and RET pathways in regulating cell growth. Sunitinib 56-65 ret proto-oncogene Homo sapiens 137-140 24061866-6 2013 Using specific human and mouse probes for genes encoding sunitinib targets, we showed a significant relation between apoptotic tumor cell numbers and human PDGFRBeta and RET mRNA expression in liver cancer and to human VEGFR2 expression in breast cancer xenografts. Sunitinib 57-66 ret proto-oncogene Homo sapiens 170-173 24276455-6 2014 RESULTS: Sunitinib and cisplatin synergistically inhibited the growth of MZ-CRC-1 cells harboring the RET M918T activating mutation. Sunitinib 9-18 ret proto-oncogene Homo sapiens 102-105 24276455-10 2014 CONCLUSIONS: Addition of cisplatin to sunitinib potentiates apoptotic cell death and has promising preclinical activity in MTCs harboring the RET M918T oncogene. Sunitinib 38-47 ret proto-oncogene Homo sapiens 142-145 24744988-12 2014 Similarly, several marketed tyrosine kinase inhibitors (TKIs) in the US (sorafenib, sunitinib, vandetanib, cabozantinib, regorafenib) are potent RET inhibitors in vitro. Sunitinib 84-93 ret proto-oncogene Homo sapiens 145-148 23102636-5 2012 RESULTS: The minimum inhibitory concentrations (IC(min)) of sunitinib quenched its primary targets: FLT-3, VEGFR-2, and RET. Sunitinib 60-69 ret proto-oncogene Homo sapiens 120-123 23454556-8 2013 In conclusion, the present study demonstrates that the RTK inhibitor Sunitinib blocks the activation of HSC and angiogenesis suggesting its potential as a drug candidate in pathological conditions like liver fibrosis and hepatocellular carcinoma. Sunitinib 69-78 ret proto-oncogene Homo sapiens 55-58 23544171-12 2013 Importantly, phospho-RTK arrays revealed novel targets for cediranib and sunitinib therapy. Sunitinib 73-82 ret proto-oncogene Homo sapiens 21-24 30349606-6 2013 Motesanib, sorafenib, vandetanib, sunitinib, lenvatinib, imatinib and cabozantinib are multi-kinase inhibitors that have the ability of inhibiting the rearranged during transection (RET) and vascular endothelial growth factor receptor (VEGFR), and other kinases, and have been used in advanced differentiated thyroid carcinoma. Sunitinib 34-43 ret proto-oncogene Homo sapiens 182-185 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 ret proto-oncogene Homo sapiens 187-190 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 ret proto-oncogene Homo sapiens 207-210 22866542-0 2012 Structural and functional analysis of KIT gene encoding receptor tyrosine kinase and its interaction with sunitinib and HDAC inhibitors: an in silico approach. Sunitinib 106-115 ret proto-oncogene Homo sapiens 56-80 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 ret proto-oncogene Homo sapiens 206-209 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 ret proto-oncogene Homo sapiens 210-213 22442268-3 2012 DESIGN: The effect of activating somatic mutations in the KRAS and BRAF genes on the responsiveness to sunitinib was evaluated in a panel of thyroid cancer cell lines harboring wild-type KRAS and BRAF genes, the RET/PTC1 rearrangement, the G12R KRAS, or the V600E BRAF mutation. Sunitinib 103-112 ret proto-oncogene Homo sapiens 212-215 22442268-4 2012 RESULTS: Sunitinib was found to selectively inhibit cell proliferation, induce cell accumulation in the G0-G1 phase, and inhibit the phosphorylation of ERK1/2 in both KRAS/BRAF wild-type thyroid cancer cells and in tumor cells harboring the RET/PTC rearrangement, whereas it was completely ineffective in KRAS- or BRAF-mutated thyroid carcinoma cells. Sunitinib 9-18 ret proto-oncogene Homo sapiens 241-244 22442268-4 2012 RESULTS: Sunitinib was found to selectively inhibit cell proliferation, induce cell accumulation in the G0-G1 phase, and inhibit the phosphorylation of ERK1/2 in both KRAS/BRAF wild-type thyroid cancer cells and in tumor cells harboring the RET/PTC rearrangement, whereas it was completely ineffective in KRAS- or BRAF-mutated thyroid carcinoma cells. Sunitinib 9-18 ret proto-oncogene Homo sapiens 245-248 21455800-11 2012 Combined treatment with sunitinib malate and docetaxel had a greater therapeutic effect than monotherapy, and the first sequential scheduling was more effective than concurrent scheduling, which partly due to the effect of docetaxel on receptor tyrosine kinase (RTK) signaling pathway. Sunitinib 24-40 ret proto-oncogene Homo sapiens 236-260 21455800-11 2012 Combined treatment with sunitinib malate and docetaxel had a greater therapeutic effect than monotherapy, and the first sequential scheduling was more effective than concurrent scheduling, which partly due to the effect of docetaxel on receptor tyrosine kinase (RTK) signaling pathway. Sunitinib 24-40 ret proto-oncogene Homo sapiens 262-265 22191389-2 2012 The multikinase inhibitor Sunitinib has been shown to inhibit the kinase activity of the RET oncogene and reduce proliferation in differentiated thyroid cancer cells harboring the RET/PTC rearrangement. Sunitinib 26-35 ret proto-oncogene Homo sapiens 89-92 22191389-2 2012 The multikinase inhibitor Sunitinib has been shown to inhibit the kinase activity of the RET oncogene and reduce proliferation in differentiated thyroid cancer cells harboring the RET/PTC rearrangement. Sunitinib 26-35 ret proto-oncogene Homo sapiens 180-183 21725210-0 2011 Sunitinib inhibits papillary thyroid carcinoma with RET/PTC rearrangement but not BRAF mutation. Sunitinib 0-9 ret proto-oncogene Homo sapiens 52-55 21725210-0 2011 Sunitinib inhibits papillary thyroid carcinoma with RET/PTC rearrangement but not BRAF mutation. Sunitinib 0-9 ret proto-oncogene Homo sapiens 56-59 21725210-4 2011 Cell growth of papillary thyroid cancer cells with RET/PTC rearrangement was effectively inhibited at low doses of sunitinib (IC50=0.658 muM), whereas that of BRAF mutated cells required higher doses. Sunitinib 115-124 ret proto-oncogene Homo sapiens 51-54 21725210-4 2011 Cell growth of papillary thyroid cancer cells with RET/PTC rearrangement was effectively inhibited at low doses of sunitinib (IC50=0.658 muM), whereas that of BRAF mutated cells required higher doses. Sunitinib 115-124 ret proto-oncogene Homo sapiens 55-58 21725210-8 2011 We conclude that sunitinib effectively inhibits RET/PTC rearrangement cells but not BRAF mutated cells. Sunitinib 17-26 ret proto-oncogene Homo sapiens 48-51 21725210-8 2011 We conclude that sunitinib effectively inhibits RET/PTC rearrangement cells but not BRAF mutated cells. Sunitinib 17-26 ret proto-oncogene Homo sapiens 52-55 21242589-13 2011 CONCLUSIONS: We confirm the clinical efficacy of sunitinib in ASPS, mediated by PDGFRB, VEGFR2, and RET, which are all expressed in tumor cells. Sunitinib 49-58 ret proto-oncogene Homo sapiens 100-103 21469976-2 2011 Sunitinib is an oral multitargeted inhibitor of vascular endothelial growth factor receptors (VEGFRs-1, -2, and -3), platelet-derived growth factor receptors (PDGFRs-alpha and -beta), stem-cell factor receptor (KIT), FMS-like tyrosine kinase 3 (FLT3), colony-stimulating factor 1 receptor (CSF-1R), and glial cell line-derived neurotrophic factor receptor (REarranged during Transfection; RET). Sunitinib 0-9 ret proto-oncogene Homo sapiens 389-392 19900123-2 2010 The receptor tyrosine kinase (RTK) inhibitor imatinib mesylate has been approved as the first-line choice of therapy for this group of patients, while the RTK inhibitor, sunitinib malate, has been approved for the treatment of GIST after disease progression or intolerance to imatinib. Sunitinib 170-186 ret proto-oncogene Homo sapiens 155-158 21325074-2 2011 Sunitinib, a potent inhibitor of RET, VEGF receptor (VEGFR)-1, VEGFR-2, VEGFR-3, and platelet-derived growth factor receptor (PDGFR)alpha/beta, has been reported as clinically effective in some patients with advanced MTC. Sunitinib 0-9 ret proto-oncogene Homo sapiens 33-36 21325074-4 2011 EXPERIMENTAL DESIGN: Both in vitro and in vivo assays, using the human TT RET(C634W) MTC cell line, were done to assess the activity of sunitinib. Sunitinib 136-145 ret proto-oncogene Homo sapiens 74-77 21325074-6 2011 RESULTS: Sunitinib displayed antiproliferative and antiangiogenic activities and inhibited RET autophosphorylation and activation of downstream signaling pathways. Sunitinib 9-18 ret proto-oncogene Homo sapiens 91-94 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 ret proto-oncogene Homo sapiens 201-204 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 ret proto-oncogene Homo sapiens 201-204 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 ret proto-oncogene Homo sapiens 201-204 20629553-2 2010 The objective of this study was to determine the effects of sunitinib on signal transduction pathways and on gene expression of iodide-metabolizing proteins in papillary cancer cells with the RET/PTC1 rearrangement. Sunitinib 60-69 ret proto-oncogene Homo sapiens 192-195 20629553-4 2010 RESULTS: Sunitinib inhibited proliferation of RET/PTC1 subclones in a time- and dose-related manner. Sunitinib 9-18 ret proto-oncogene Homo sapiens 46-49 20629553-6 2010 Incubation of RET/PTC1 cells with 1 microM sunitinib inhibited their migration potential and transformed their morphology. Sunitinib 43-52 ret proto-oncogene Homo sapiens 14-17 20629553-7 2010 Sunitinib inhibited RET autophosphorylation at Y1062 and the activation of signal transducer and activator of transcription 3 by blocking Y705 phosphorylation. Sunitinib 0-9 ret proto-oncogene Homo sapiens 20-23 20629553-10 2010 Sunitinib treatment of RET/PTC1 cell lines, in combination, with forskolin induced expression of the sodium (Na)/iodide (I) symporter (NIS) and the transcription factors that bind the NIS upstream enhancer. Sunitinib 0-9 ret proto-oncogene Homo sapiens 23-26 20629553-12 2010 CONCLUSION: Sunitinib appears to target the cytosolic MEK/ERK and SAPK/JNK pathways in the RET/PTC1 cell lines, suggesting that blocking these pathways is at least part of the mechanism by which sunitinib inhibits cell proliferation and causes stimulation of NIS gene expression in RET/PTC1 cells. Sunitinib 12-21 ret proto-oncogene Homo sapiens 91-94 20629553-12 2010 CONCLUSION: Sunitinib appears to target the cytosolic MEK/ERK and SAPK/JNK pathways in the RET/PTC1 cell lines, suggesting that blocking these pathways is at least part of the mechanism by which sunitinib inhibits cell proliferation and causes stimulation of NIS gene expression in RET/PTC1 cells. Sunitinib 12-21 ret proto-oncogene Homo sapiens 282-285 19649772-1 2010 BACKGROUND: Sunitinib is an orally administered multitargeted tyrosine kinase inhibitor of RET, VEGFR, PDGFR, and c-KIT. Sunitinib 12-21 ret proto-oncogene Homo sapiens 91-94 20696054-6 2010 Genes whose protein products are targeted by the RET inhibitors sunitinib and sorafenib correlated with being amplified and or highly expressed. Sunitinib 64-73 ret proto-oncogene Homo sapiens 49-52 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 ret proto-oncogene Homo sapiens 229-232 19453268-3 2009 Sunitinib is a multi-kinase inhibitor of VEGFR-2, PDGFR (alpha,beta), FLT-3, KIT, CSF-1 and RET. Sunitinib 0-9 ret proto-oncogene Homo sapiens 92-95 19894779-0 2009 Sunitinib: a multitargeted receptor tyrosine kinase inhibitor in the era of molecular cancer therapies. Sunitinib 0-9 ret proto-oncogene Homo sapiens 27-51 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 ret proto-oncogene Homo sapiens 142-145 19468197-6 2009 While such tyrosine kinase inhibitors, particularly those affecting RET activity such as vandetanib, sorafenib and sunitinib, are promising, the low rate of partial responses and absence of complete responses in all of the various trials of monotherapy emphasize the need for new and more effective single agents or combinations of therapeutic agents with acceptable toxicity. Sunitinib 115-124 ret proto-oncogene Homo sapiens 68-71 18418222-3 2008 Sunitinib is active against the RET kinase and has both antineoplastic and antiangiogenic properties. Sunitinib 0-9 ret proto-oncogene Homo sapiens 32-35 17505827-1 2008 PURPOSE: Sunitinib, an oral multitargeted tyrosine kinase inhibitor that inhibits VEGFR, PDGFR, FLT3, KIT, and RET, is currently approved for the treatment of imatinib-refractory GIST and advanced renal cell carcinoma at a dose of 50 mg daily for 4 weeks followed by a 2-week off period (4/2 schedule). Sunitinib 9-18 ret proto-oncogene Homo sapiens 111-114 17945482-1 2008 SU11248 sunitinib malate sutent is a selective inhibitor of certain protein tyrosine kinases including VEGF-R types 1-3 PDGF-R-a and -b, c-kit, and RET. Sunitinib 0-7 ret proto-oncogene Homo sapiens 148-151 18537751-7 2008 Currently, the sole approved second-line drug is sunitinib--a multitargeted agent, an inhibitor of tyrosine kinase, of KIT and PDGFRA/B and of the vascular endothelial growth factor receptors (VEGFRs)-1, -2 and 3, FMS-like tyrosine kinase-3 (FLT3), colony stimulating factor 1 receptor (CSF-1R), and glial cell-line derived neurotrophic factor receptor (REarranged during Transfection; RET). Sunitinib 49-58 ret proto-oncogene Homo sapiens 386-389