PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 28327411-3 2017 Gas6-induced Axl signaling in presence of Sunitinib is also diversified displaying onset of Axl-dependent EGFR and METR activation and activation of classical MAPK pathways. Sunitinib 42-51 epidermal growth factor receptor Homo sapiens 106-110 31054432-7 2019 IC50 of the promising compounds were in the range of 247-793 nM for VEGFR-2 in reference to sunitinib (IC50 320 nM), and 369-725 nM for EGFR in reference to erlotinib (IC50 568 nM). Sunitinib 92-101 epidermal growth factor receptor Homo sapiens 69-73 31035254-8 2019 Therefore, we evaluated with AlphaScreen technology the phosphorylated EGFR and IGF1R levels in primary cultures treated with sunitinib and/or EGF and IGF1. Sunitinib 126-135 epidermal growth factor receptor Homo sapiens 71-75 27706901-5 2016 These data, together with molecular docking simulations, revealed distinct differences in the impact of structural modifications on drug binding to the enzymes: whereas the catalytic pocket of the epidermal growth factor receptor (EGFR) accepted all new erlotinib derivatives, the vascular endothelial growth factor receptor (VEGFR)-inhibitory potential in the case of the sunitinib prodrugs was dramatically diminished by derivatization. Sunitinib 373-382 epidermal growth factor receptor Homo sapiens 197-229 27706901-5 2016 These data, together with molecular docking simulations, revealed distinct differences in the impact of structural modifications on drug binding to the enzymes: whereas the catalytic pocket of the epidermal growth factor receptor (EGFR) accepted all new erlotinib derivatives, the vascular endothelial growth factor receptor (VEGFR)-inhibitory potential in the case of the sunitinib prodrugs was dramatically diminished by derivatization. Sunitinib 373-382 epidermal growth factor receptor Homo sapiens 231-235 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 epidermal growth factor receptor Homo sapiens 37-41 27016208-0 2016 Schedule-dependent cytotoxicity of sunitinib and TRAIL in human non-small cell lung cancer cells with or without EGFR and KRAS mutations. Sunitinib 35-44 epidermal growth factor receptor Homo sapiens 113-117 26484875-2 2015 Clinical trials enrolling ACC patients with high tissue vascular endothelial growth factor receptor (VEGFR) expression levels showed controversial results after treatment with Sunitinib, possibly due to variability in the expression of drug targets, which include epidermal growth factor receptor (EGFR). Sunitinib 176-185 epidermal growth factor receptor Homo sapiens 264-296 26934000-5 2016 The combination of the ERBB1/2/4 inhibitor afatinib with the SRC family inhibitor dasatinib killed afatinib resistant H1975 cells in a greater than additive fashion; other drugs used in combination with dasatinib such as sunitinib, crizotinib and amufatinib were less effective. Sunitinib 221-230 epidermal growth factor receptor Homo sapiens 23-32 26484875-2 2015 Clinical trials enrolling ACC patients with high tissue vascular endothelial growth factor receptor (VEGFR) expression levels showed controversial results after treatment with Sunitinib, possibly due to variability in the expression of drug targets, which include epidermal growth factor receptor (EGFR). Sunitinib 176-185 epidermal growth factor receptor Homo sapiens 102-106 26484875-5 2015 In addition, by cell viability, proliferation and caspase activation assays we found that Sunitinib inhibits adrenocortical cell viability acting, at least in part, through EGFR, that, in turn, is crucial for EGF proliferative effect on adrenocortical cells. Sunitinib 90-99 epidermal growth factor receptor Homo sapiens 173-177 25971960-11 2015 Both ERalpha-positive and low-EGFR-expressing tumors had an increased in vitro sunitinib response, as determined by alteration of Erk activation. Sunitinib 79-88 epidermal growth factor receptor Homo sapiens 30-34 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 epidermal growth factor receptor Homo sapiens 106-110 26306766-0 2015 Induction of epithelial-mesenchymal transition via activation of epidermal growth factor receptor contributes to sunitinib resistance in human renal cell carcinoma cell lines. Sunitinib 113-122 epidermal growth factor receptor Homo sapiens 65-97 26306766-3 2015 We aimed to study the association between sunitinib sensitivity and epithelial-mesenchymal transition (EMT) regulation via epidermal growth factor receptor (EGFR) signaling, which is a mechanism of resistance to anticancer drugs. Sunitinib 42-51 epidermal growth factor receptor Homo sapiens 123-155 26306766-3 2015 We aimed to study the association between sunitinib sensitivity and epithelial-mesenchymal transition (EMT) regulation via epidermal growth factor receptor (EGFR) signaling, which is a mechanism of resistance to anticancer drugs. Sunitinib 42-51 epidermal growth factor receptor Homo sapiens 157-161 26306766-6 2015 After treatment with sunitinib, EGFR phosphorylation increased in 786-O cells, resulting in an increase in the phosphorylation of extracellular signal-regulated kinase, nuclear translocation of beta-catenin, and expression of mesenchymal markers. Sunitinib 21-30 epidermal growth factor receptor Homo sapiens 32-36 26306766-7 2015 These results suggest that sunitinib induced EMT via activation of EGFR in 786-O cells, but not in ACHN and Caki-1 cells. Sunitinib 27-36 epidermal growth factor receptor Homo sapiens 67-71 26306766-8 2015 Caki-1/SN cells, a resistant cell line generated by continuous exposure to sunitinib, displayed increased phosphorylation of EGFR. Sunitinib 75-84 epidermal growth factor receptor Homo sapiens 125-129 26306766-9 2015 Cell viability in the presence of sunitinib was decreased by erlotinib, as the selective inhibitor of EGFR, treatment in 786-O and Caki-1/SN cells. Sunitinib 34-43 epidermal growth factor receptor Homo sapiens 102-106 26306766-10 2015 Similarly, erlotinib suppressed sunitinib-induced EGFR activation and upregulated mesenchymal markers. Sunitinib 32-41 epidermal growth factor receptor Homo sapiens 50-54 26306766-11 2015 Thus, we postulate that resistance to sunitinib in RCC may be associated with EMT caused by activation of EGFR. Sunitinib 38-47 epidermal growth factor receptor Homo sapiens 106-110 24118906-0 2014 The evaluation of efficacy and safety of sunitinib on EGFR-TKI pretreated advanced non-small cell lung cancer patients in China. Sunitinib 41-50 epidermal growth factor receptor Homo sapiens 54-58 20558072-4 2010 Remarkably, dimethylation of both the 4-N and N7 afford whole cell EGFR inhibitors that are more cytotoxic than clinically used erlotinib and mono-methylation at the 4-N or N7 affords more cytotoxic whole cell PDGFR-beta inhibitors than clinically used sunitinib. Sunitinib 253-262 epidermal growth factor receptor Homo sapiens 67-71 21796416-0 2011 Synergistic interaction between sunitinib and docetaxel is sequence dependent in human non-small lung cancer with EGFR TKIs-resistant mutation. Sunitinib 32-41 epidermal growth factor receptor Homo sapiens 114-118 21796416-10 2011 CONCLUSIONS: Sunitinib as a single agent exhibits anti-proliferative effects in vitro in NSCLC cell lines with EGFR T790M and K-ras mutations but the sequential administration of docetaxel followed by sunitinib is superior to sunitinib followed by docetaxel and concurrent administration. Sunitinib 13-22 epidermal growth factor receptor Homo sapiens 111-115 22819259-3 2012 In the present study, we demonstrate that the tyrosine kinase receptor inhibitor Sunitinib reduces cell viability, proliferation, clonogenicity and induces apoptotic cell death in endometrial carcinoma cell lines, which is not due to its action through the most known targets like VEGFR, nor through EGFR as demonstrated in this work. Sunitinib 81-90 epidermal growth factor receptor Homo sapiens 282-286 23056179-8 2012 However, the in vivo efficacy testing of the gefitinib and sunitinib combination in an EGFR amplified/PTEN wild type GBM xenograft model revealed that gefitinib alone could significantly improve survival in animals whereas sunitinib did not show any survival benefit. Sunitinib 59-68 epidermal growth factor receptor Homo sapiens 87-91 20524040-4 2011 Daoy and D556 human medulloblastoma cells pre-treated for 1 h with 0.2 muM sunitinib demonstrated induction of PTEN expression and significant inhibition of PDGFR signaling activity and transactivation of EGFR, in a RAS-independent manner, in response to PDGF-BB stimulation. Sunitinib 75-84 epidermal growth factor receptor Homo sapiens 205-209 21187479-1 2010 OBJECTIVE: The aim of this study was to assess the antitumour effect of an anti-VEGFR (sunitinib) and the anti-EGFR multi-targeted agent (lapatinib), applied either alone or in combination on the migration capacity of two glioma cell lines. Sunitinib 87-96 epidermal growth factor receptor Homo sapiens 81-85 21187479-11 2010 CONCLUSION: The preliminary results of this study are the first to support the implication of a dual anti-EGFR/HER-2 agent, lapatinib and a multi-targeted agent, sunitinib in glioma cell migration, through a mechanism implying interruption of growth factor receptor integrin complexes formation. Sunitinib 162-171 epidermal growth factor receptor Homo sapiens 106-110 16046538-6 2005 The KIT/FLT3 inhibitor SU-11248 potently inhibits the imatinib-resistant KIT(V559D/T670I) kinase, consistent with the clinical efficacy of SU-11248 against imatinib-resistant gastrointestinal tumors, and the EGFR inhibitors EKB-569 and CI-1033, but not GW-572016 and ZD-6474, potently inhibit the gefitinib- and erlotinib-resistant EGFR(L858R/T790M) kinase. Sunitinib 23-31 epidermal growth factor receptor Homo sapiens 208-212 16046538-6 2005 The KIT/FLT3 inhibitor SU-11248 potently inhibits the imatinib-resistant KIT(V559D/T670I) kinase, consistent with the clinical efficacy of SU-11248 against imatinib-resistant gastrointestinal tumors, and the EGFR inhibitors EKB-569 and CI-1033, but not GW-572016 and ZD-6474, potently inhibit the gefitinib- and erlotinib-resistant EGFR(L858R/T790M) kinase. Sunitinib 23-31 epidermal growth factor receptor Homo sapiens 332-336 35165100-6 2022 pTyr-phosphoproteomic profiles of tumor samples from 4 sunitinib-treated versus 7 control patients revealed 108 significantly up- and 23 downregulated (p<0.05) phosphopeptides for sunitinib-treatment, resulting in an EGFR-centered signaling network. Sunitinib 180-189 epidermal growth factor receptor Homo sapiens 217-221 33170322-1 2021 The objective of present work is to evaluate possible interactions among four clinically-used vascular epidermal growth factor receptor (VEGFR)-tyrosine kinase inhibitors (TKIs), including apatinib, cabozantinib, sorafenib, and sunitinib, with epidermal growth factor receptor (EGFR)-TKI gefitinib. Sunitinib 228-237 epidermal growth factor receptor Homo sapiens 103-135