PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 27461627-10 2016 Compared with the control group, both the MDR1 and VEGF mRNA decreased in a dose-dependent manner following 48 hours of treatment of octreotide (P < 0.05). Octreotide 133-143 vascular endothelial growth factor A Homo sapiens 51-55 27461627-11 2016 The results of western blot showed that octreotide decreased the expressions of SSTR2, MDR1, and VEGF protein in a dose-dependent manner (P < 0.05). Octreotide 40-50 vascular endothelial growth factor A Homo sapiens 97-101 23525276-8 2013 The levels of ET-1 and collagen I in the supernatant decreased significantly in contrast with the normal levels, whereas the levels of VEGF in the LX-2 cells and the supernatant increased at a high octreotide concentration (10-5 nM). Octreotide 198-208 vascular endothelial growth factor A Homo sapiens 135-139 24632829-10 2014 There was obvious increase in caspase 3 expression in the OCT alone and two-drug combined treatment groups, however, VEGFA expression was markedly suppressed in them. Octreotide 58-61 vascular endothelial growth factor A Homo sapiens 117-122 23525276-9 2013 Octreotide may exert its effects on ET-1 or other targeting genes in HSCs through the downregulation of c-Jun and specificity protein 1 (sp-1), and the increased levels of VEGF may be the reason for the side effects observed at high concentrations of octreotide. Octreotide 251-261 vascular endothelial growth factor A Homo sapiens 172-176 21822978-5 2012 Reducing tumor angiogenesis by combining the somatostatin analog octreotide with small doses of heparin is one approach in decreasing metastasis rates by targeting VEGF and heparinase, respectively. Octreotide 65-75 vascular endothelial growth factor A Homo sapiens 164-168 21677423-4 2011 RESULTS: 10(-8)M octreotide markedly inhibited both basal and VEGF-stimulated HUVEC proliferation, had no effect on endothelial cell migration, but inhibited endothelial tubule formation. Octreotide 17-27 vascular endothelial growth factor A Homo sapiens 62-66 22572824-2 2012 This trial explored whether octreotide, an inhibitor of vascular endothelial growth factor, a putative mediator of ascites, prolongs the interval to next paracentesis. Octreotide 28-38 vascular endothelial growth factor A Homo sapiens 56-90 19478472-6 2009 Moreover, intratumoral angiogenesis quantified by microvessel density as well as serum and tissue vascular endothelial growth factor (VEGF) levels were considerably decreased in octreotide-treated animals compared to the control animals. Octreotide 178-188 vascular endothelial growth factor A Homo sapiens 98-132 19478472-6 2009 Moreover, intratumoral angiogenesis quantified by microvessel density as well as serum and tissue vascular endothelial growth factor (VEGF) levels were considerably decreased in octreotide-treated animals compared to the control animals. Octreotide 178-188 vascular endothelial growth factor A Homo sapiens 134-138 19478472-7 2009 These findings suggest that octreotide may prevent the occurrence of second primary hepatomas and lung metastasis after resection of primary HCC, which may be partially attributed to down-regulation of VEGF and subsequent reduction in tumor angiogenesis. Octreotide 28-38 vascular endothelial growth factor A Homo sapiens 202-206 12969536-7 2003 RESULTS: After a week of Sandostatin therapy,the concentration of VEGF and bFGF in serum was drastically diminished (VEGF:1.02+/-0.41 microg /L vs 1.88+/-0.87 microg/L, P< 0.05;bFGF:0.88+/-0.32 ng/L vs 2.12+/-1.06 ng/L,P< 0.05). Octreotide 25-36 vascular endothelial growth factor A Homo sapiens 66-70 18953743-0 2008 Expression of vascular endothelial growth factor in growth hormone-secreting pituitary adenomas: special reference to the octreotide treatment. Octreotide 122-132 vascular endothelial growth factor A Homo sapiens 14-48 18953743-1 2008 OBJECTIVE: The present study was designed to investigate the localization of VEGF in GH-secreting pituitary adenomas and to evaluate the characteristic differences of VEGF expression in relation to the clinical effect of preoperative treatment with octreotide. Octreotide 249-259 vascular endothelial growth factor A Homo sapiens 167-171 18953743-10 2008 Moderately positive staining with VEGF appeared in six of 33 (18%) cases of the octreotide group, and in eight of 12 (67%) cases of the control group. Octreotide 80-90 vascular endothelial growth factor A Homo sapiens 34-38 18953743-15 2008 CONCLUSION: We conclude that octreotide may inhibit the angiogenesis through down-regulation of VEGF. Octreotide 29-39 vascular endothelial growth factor A Homo sapiens 96-100 15381031-7 2004 Somatostatin and octreotide, a somatostatin analogue, inhibited IGF-1 receptor (IGF-1R) phosphorylation and decreased VEGF production. Octreotide 17-27 vascular endothelial growth factor A Homo sapiens 118-122 15381031-8 2004 Both IGF-1R phosphorylation and accumulation of VEGF mRNA were inhibited by physiological levels of somatostatin and octreotide (1 nM). Octreotide 117-127 vascular endothelial growth factor A Homo sapiens 48-52 15381031-9 2004 These results demonstrate somatostatin and octreotide mediated attenuation of both IGF-1R signal transduction and VEGF mRNA accumulation via somatostatin receptor type 2 (sst2). Octreotide 43-53 vascular endothelial growth factor A Homo sapiens 114-118 18636202-0 2008 Vascular endothelial growth factor monitoring in advanced hepatocellular carcinoma patients treated with radiofrequency ablation plus octreotide: a single center experience. Octreotide 134-144 vascular endothelial growth factor A Homo sapiens 0-34 12969536-7 2003 RESULTS: After a week of Sandostatin therapy,the concentration of VEGF and bFGF in serum was drastically diminished (VEGF:1.02+/-0.41 microg /L vs 1.88+/-0.87 microg/L, P< 0.05;bFGF:0.88+/-0.32 ng/L vs 2.12+/-1.06 ng/L,P< 0.05). Octreotide 25-36 vascular endothelial growth factor A Homo sapiens 117-121 12969536-10 2003 CONCLUSION: By the short-term therapy of sandostatin, the expression of VEGF and bFGF can be inhibited. Octreotide 41-52 vascular endothelial growth factor A Homo sapiens 72-76 11304689-3 2001 Cultivated cells from solid human gliomas of different stages and glioma cell lines secreted variable amounts of VEGF, which could be lowered to 25% to 80% by co-incubation with somatostatin or sst2-selective agonists (octreotide and L-054,522). Octreotide 219-229 vascular endothelial growth factor A Homo sapiens 113-117 12811549-2 2003 METHODS: Using MTT assay, invasion assay, migration assay, and Matrigel assay, the effects of octreotide on endothelial cells stimulated by vascular endothelial growth factor (VEGF) were evaluated in vitro. Octreotide 94-104 vascular endothelial growth factor A Homo sapiens 140-174 12811549-2 2003 METHODS: Using MTT assay, invasion assay, migration assay, and Matrigel assay, the effects of octreotide on endothelial cells stimulated by vascular endothelial growth factor (VEGF) were evaluated in vitro. Octreotide 94-104 vascular endothelial growth factor A Homo sapiens 176-180 12811549-8 2003 RESULTS: In vitro, octreotide inhibited the proliferation, invasion, and differentiation of HUVECs elicited by VEGF. Octreotide 19-29 vascular endothelial growth factor A Homo sapiens 111-115 11953120-13 2002 The VEGF and MMP-2 expression was inhibited by octreotide. Octreotide 47-57 vascular endothelial growth factor A Homo sapiens 4-8 12239460-12 2002 The plasma levels of VEGF and bFGF were reduced by octreotide. Octreotide 51-61 vascular endothelial growth factor A Homo sapiens 21-25 32829374-8 2020 RESULTS Octreotide-paclitaxel conjugate inhibited phosphorylation of the p38MAPK signal pathway, decreased the expression of downstream VEGF, and increased the apoptosis of drug-resistant cancer cells. Octreotide 8-18 vascular endothelial growth factor A Homo sapiens 136-140 11291560-0 2001 Inhibition of vascular endothelial growth factor by octreotide in colorectal cancer patients. Octreotide 52-62 vascular endothelial growth factor A Homo sapiens 14-48 11291560-4 2001 Effects of octreotide on VEGF expression were evaluated in 35 patients with operable colorectal cancer receiving octreotide for 2 weeks before surgery. Octreotide 11-21 vascular endothelial growth factor A Homo sapiens 25-29 11291560-8 2001 The present study indicates that octreotide inhibits expression of VEGF in colorectal cancer patients, and, furthermore, that serum VEGF expression correlates with tissue VEGF, representing a safe method to monitor the activity of antiangiogenic agents. Octreotide 33-43 vascular endothelial growth factor A Homo sapiens 67-71 30895501-8 2019 Octreotide-induced VEGF alterations analyzed by the antibody array and by ELISA were not fully matched. Octreotide 0-10 vascular endothelial growth factor A Homo sapiens 19-23