PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 16942942-1 2006 BACKGROUND: Although aspirin is useful in reducing platelet activation and cardiovascular events, its effects on platelet levels of angiogenic factors, such as vascular endothelial growth factor (VEGF) and angiopoietin-1 (Ang-1), and markers of platelet activation in hypertension are unknown. Aspirin 21-28 vascular endothelial growth factor A Homo sapiens 160-194 18544566-0 2008 NO-donating aspirin inhibits angiogenesis by suppressing VEGF expression in HT-29 human colon cancer mouse xenografts. Aspirin 12-19 vascular endothelial growth factor A Homo sapiens 57-61 18544566-7 2008 The expression of vascular endothelial growth factor (VEGF) was significantly reduced in response to NO-ASA, with the p- isomer being more potent than the m-. Aspirin 104-107 vascular endothelial growth factor A Homo sapiens 18-52 18544566-7 2008 The expression of vascular endothelial growth factor (VEGF) was significantly reduced in response to NO-ASA, with the p- isomer being more potent than the m-. Aspirin 104-107 vascular endothelial growth factor A Homo sapiens 54-58 18544566-8 2008 NO-ASA altered the spatial distribution of VGEF expression, with 16.7% of the vehicle-treated xenografts displaying diminished VEGF in the inner region of the area between necrosis and the outer perimeter of the tumor, compared with those treated with m- (58.3%) or p-NO-ASA (75%, P < 0.01 for both versus control). Aspirin 3-6 vascular endothelial growth factor A Homo sapiens 127-131 18483373-7 2008 In univariate analysis, aspirin use attenuated the tamoxifen-associated increase in VEGF in the platelet releasate and decreased serum levels of VEGF (P = 0.03). Aspirin 24-31 vascular endothelial growth factor A Homo sapiens 84-88 18483373-7 2008 In univariate analysis, aspirin use attenuated the tamoxifen-associated increase in VEGF in the platelet releasate and decreased serum levels of VEGF (P = 0.03). Aspirin 24-31 vascular endothelial growth factor A Homo sapiens 145-149 18193074-0 2008 ATL-1, an analogue of aspirin-triggered lipoxin A4, is a potent inhibitor of several steps in angiogenesis induced by vascular endothelial growth factor. Aspirin 22-29 vascular endothelial growth factor A Homo sapiens 118-152 18193074-2 2008 We have demonstrated that ATL-1, a synthetic analogue of aspirin-triggered lipoxin A(4), inhibits VEGF-induced endothelial cell (EC) migration. Aspirin 57-64 vascular endothelial growth factor A Homo sapiens 98-102 18001701-5 2008 The effects of a 6-month treatment with aspirin 100 mg/day on VEGF levels of 20 hypertensive patients were also studied. Aspirin 40-47 vascular endothelial growth factor A Homo sapiens 62-66 18001701-8 2008 Aspirin treated hypertensives showed a significant reduction of sP-selectin (-26%, p<0.01) and VEGF (-33%, p<0.01) levels. Aspirin 0-7 vascular endothelial growth factor A Homo sapiens 98-102 18001701-10 2008 CONCLUSIONS: In vivo activation of platelets in hypertensive patients is responsible for enhanced circulating VEGF levels, which are significantly lowered by aspirin treatment. Aspirin 158-165 vascular endothelial growth factor A Homo sapiens 110-114 16942942-7 2006 After treatment with aspirin for 3 months, there were significant reductions in plasma VEGF (P=.01), pAng-1 (P=.04), sPsel (P=.001), and pPsel (P<.001) levels, but not levels of platelet VEGF and plasma Ang-1. Aspirin 21-28 vascular endothelial growth factor A Homo sapiens 87-91 16942942-7 2006 After treatment with aspirin for 3 months, there were significant reductions in plasma VEGF (P=.01), pAng-1 (P=.04), sPsel (P=.001), and pPsel (P<.001) levels, but not levels of platelet VEGF and plasma Ang-1. Aspirin 21-28 vascular endothelial growth factor A Homo sapiens 190-194 16132039-0 2006 Aspirin-triggered Lipoxin A4 inhibition of VEGF-induced endothelial cell migration involves actin polymerization and focal adhesion assembly. Aspirin 0-7 vascular endothelial growth factor A Homo sapiens 43-47 16132039-2 2006 We demonstrated previously that an aspirin-triggered lipoxin analog, 15-epi-16-(para-fluoro)-phenoxy-lipoxin A4 (ATL-1), inhibits vascular endothelial growth factor (VEGF)-induced EC migration. Aspirin 35-42 vascular endothelial growth factor A Homo sapiens 130-164 16132039-2 2006 We demonstrated previously that an aspirin-triggered lipoxin analog, 15-epi-16-(para-fluoro)-phenoxy-lipoxin A4 (ATL-1), inhibits vascular endothelial growth factor (VEGF)-induced EC migration. Aspirin 35-42 vascular endothelial growth factor A Homo sapiens 166-170 14521608-0 2003 Aspirin and salicylate inhibit colon cancer medium- and VEGF-induced endothelial tube formation: correlation with suppression of cyclooxygenase-2 expression. Aspirin 0-7 vascular endothelial growth factor A Homo sapiens 56-60 14996470-0 2004 Aspirin decreases vascular endothelial growth factor release during myocardial ischemia. Aspirin 0-7 vascular endothelial growth factor A Homo sapiens 18-52 14996470-6 2004 RESULTS: Vascular Endothelial Growth Factor levels were significantly lower in patients of the aspirin group compared to those of the non-aspirin group; 94+/-61 vs. 241+/-118 pg/ml, p=0.0003, respectively, this-despite an absence of difference in the platelet count between the groups. Aspirin 95-102 vascular endothelial growth factor A Homo sapiens 9-43 14996470-6 2004 RESULTS: Vascular Endothelial Growth Factor levels were significantly lower in patients of the aspirin group compared to those of the non-aspirin group; 94+/-61 vs. 241+/-118 pg/ml, p=0.0003, respectively, this-despite an absence of difference in the platelet count between the groups. Aspirin 138-145 vascular endothelial growth factor A Homo sapiens 9-43 14996470-11 2004 CONCLUSIONS: Aspirin treated patients have lower Vascular Endothelial Growth Factor titer levels in the perioperative course. Aspirin 13-20 vascular endothelial growth factor A Homo sapiens 49-83 14521608-7 2003 Aspirin or sodium salicylate inhibited VEGF-induced tube formation in a concentration-dependent manner comparable to that of inhibition of colon cancer medium-induced endothelial tube formation. Aspirin 0-7 vascular endothelial growth factor A Homo sapiens 39-43 14521608-10 2003 Furthermore, aspirin and sodium salicylate inhibited COX-2 expression stimulated by VEGF. Aspirin 13-20 vascular endothelial growth factor A Homo sapiens 84-88 11376496-8 2001 Secretion of PDGF-AB and VEGF increased during the first days of low dose aspirin exposition; higher concentrations led to a depletion of cytokines after an initial liberation in the case of VEGF, mRNA of which was also dose-dependently increased by aspirin. Aspirin 74-81 vascular endothelial growth factor A Homo sapiens 25-29 11376496-8 2001 Secretion of PDGF-AB and VEGF increased during the first days of low dose aspirin exposition; higher concentrations led to a depletion of cytokines after an initial liberation in the case of VEGF, mRNA of which was also dose-dependently increased by aspirin. Aspirin 250-257 vascular endothelial growth factor A Homo sapiens 191-195 30888847-17 2019 CONCLUSION:: Daily use of low-dose ASA reduces VEGF, PDGF-AB, and TGF-beta1 expression in freshly isolated human LR-PRP when activated with AA. Aspirin 35-38 vascular endothelial growth factor A Homo sapiens 47-51 33427041-9 2021 COX-independent mechanisms of anticancer effects of aspirin include down-regulation of nuclear factor kappa B activity and Akt activation, modulation of Bcl-2 and Bax family proteins, suppression of vascular endothelial growth factor, induction of apoptosis, disruption of DNA repair mechanisms, and induction of spermidine/spermine N1-acetyltransferase that modulates polyamine catabolism. Aspirin 52-59 vascular endothelial growth factor A Homo sapiens 199-233 30693272-0 2018 Aspirin Inhibits Natural Killer/T-Cell Lymphoma by Modulation of VEGF Expression and Mitochondrial Function. Aspirin 0-7 vascular endothelial growth factor A Homo sapiens 65-69 30693272-3 2018 In this study, we found that aspirin treatment suppresses VEGF expression in NKTCL SNK-6 cells. Aspirin 29-36 vascular endothelial growth factor A Homo sapiens 58-62 30693272-4 2018 Further investigation showed that aspirin treatment increases histone methylation in the range of -100~0 that is proximal to the transcription start site on the VEGF promoter, subsequently decreasing the binding ability of Sp1 to the VEGF promoter with VEGF suppression. Aspirin 34-41 vascular endothelial growth factor A Homo sapiens 161-165 30693272-4 2018 Further investigation showed that aspirin treatment increases histone methylation in the range of -100~0 that is proximal to the transcription start site on the VEGF promoter, subsequently decreasing the binding ability of Sp1 to the VEGF promoter with VEGF suppression. Aspirin 34-41 vascular endothelial growth factor A Homo sapiens 234-238 30693272-4 2018 Further investigation showed that aspirin treatment increases histone methylation in the range of -100~0 that is proximal to the transcription start site on the VEGF promoter, subsequently decreasing the binding ability of Sp1 to the VEGF promoter with VEGF suppression. Aspirin 34-41 vascular endothelial growth factor A Homo sapiens 234-238 30693272-6 2018 Aspirin treatment alone slightly inhibits NKTCL SNK-6 tumor growth and EBV replication; while in the presence of histone deacetylase inhibitor (HDACi) chidamide (CDM), aspirin significantly suppresses the VEGF signaling pathway with increased ROS overgeneration and EBV inhibition. Aspirin 0-7 vascular endothelial growth factor A Homo sapiens 205-209 30693272-6 2018 Aspirin treatment alone slightly inhibits NKTCL SNK-6 tumor growth and EBV replication; while in the presence of histone deacetylase inhibitor (HDACi) chidamide (CDM), aspirin significantly suppresses the VEGF signaling pathway with increased ROS overgeneration and EBV inhibition. Aspirin 168-175 vascular endothelial growth factor A Homo sapiens 205-209 30693272-8 2018 This is the first time that the potential mechanism for aspirin-mediated VEGF suppression and anti-tumor effect has been discovered, and this study provides a new strategy for anti-tumor drug development for NKTCL treatment based on aspirin-mediated targeting of the VEGF signaling pathway and ROS formation. Aspirin 56-63 vascular endothelial growth factor A Homo sapiens 73-77 30693272-8 2018 This is the first time that the potential mechanism for aspirin-mediated VEGF suppression and anti-tumor effect has been discovered, and this study provides a new strategy for anti-tumor drug development for NKTCL treatment based on aspirin-mediated targeting of the VEGF signaling pathway and ROS formation. Aspirin 56-63 vascular endothelial growth factor A Homo sapiens 267-271 30693272-8 2018 This is the first time that the potential mechanism for aspirin-mediated VEGF suppression and anti-tumor effect has been discovered, and this study provides a new strategy for anti-tumor drug development for NKTCL treatment based on aspirin-mediated targeting of the VEGF signaling pathway and ROS formation. Aspirin 233-240 vascular endothelial growth factor A Homo sapiens 73-77 30693272-8 2018 This is the first time that the potential mechanism for aspirin-mediated VEGF suppression and anti-tumor effect has been discovered, and this study provides a new strategy for anti-tumor drug development for NKTCL treatment based on aspirin-mediated targeting of the VEGF signaling pathway and ROS formation. Aspirin 233-240 vascular endothelial growth factor A Homo sapiens 267-271 27638860-10 2016 We also found that both aspirin-PC and aspirin have robust antineoplastic action in the presence of VEGF-blocking drugs. Aspirin 24-31 vascular endothelial growth factor A Homo sapiens 100-104 30144594-0 2018 Aspirin Affects Tumor Angiogenesis and Sensitizes Human Glioblastoma Endothelial Cells to Temozolomide, Bevacizumab, and Sunitinib, Impairing Vascular Endothelial Growth Factor-Related Signaling. Aspirin 0-7 vascular endothelial growth factor A Homo sapiens 142-176 30144594-8 2018 RESULTS: Our data reported that ASA affected GBM-EC viability, tube-like structure formation, cell migration, and VEGF releasing in a dose-dependent manner and that combined treatments with TMZ, BEV, and SUN synergized to counteract proangiogenic cell ability. Aspirin 32-35 vascular endothelial growth factor A Homo sapiens 114-118 30144594-9 2018 mRNA expression analysis displayed a marked effect of ASA in reducing VEGF, VEGFR-1, HIF-1alpha, RAS, mitogen-activated protein kinase kinase, AKT, and BCL-2, as well a combined anticancer effect of ASA together with TMZ, BEV, and SUN. Aspirin 54-57 vascular endothelial growth factor A Homo sapiens 70-74 27555316-15 2017 The vascular endothelial growth factor level was significantly higher in the letrozole-treated group than aspirin-treated group (0.49 +- 0.26 vs 0.42 +- 0.22, P = .029). Aspirin 106-113 vascular endothelial growth factor A Homo sapiens 4-38 25990653-12 2015 ASA abrogated enzastaurin-potentiated washed-platelet aggregation and VEGF release. Aspirin 0-3 vascular endothelial growth factor A Homo sapiens 70-74 25607509-0 2015 Decreased vascular endothelial growth factor expression is associated with cell apoptosis in low-dose aspirin-induced gastric mucosal injury. Aspirin 102-109 vascular endothelial growth factor A Homo sapiens 10-44 22561363-7 2012 ASA and its salicylic acid (SA) moiety both suppressed Ang II-mediated AT1R and vascular endothelial growth factor expression and the subsequent new capillary formation. Aspirin 0-3 vascular endothelial growth factor A Homo sapiens 80-114 24506800-10 2014 When acetylsalicylic acid was combined with simvastatin treatment, the intraocular levels of Ang-2 and VEGF were significantly lower than in diabetics treated with simvastatin alone. Aspirin 5-25 vascular endothelial growth factor A Homo sapiens 103-107 25479628-6 2014 The levels of VEGF-A/C/D in Danzhi decoction group and aspirin group were significantly lower than those in mock group (P<0.05), while there was no significant difference between Danzhi decoction group and aspirin group (P>0.05). Aspirin 55-62 vascular endothelial growth factor A Homo sapiens 14-20 24766194-0 2014 Aspirin inhibits proliferation and induces apoptosis of multiple myeloma cells through regulation of Bcl-2 and Bax and suppression of VEGF. Aspirin 0-7 vascular endothelial growth factor A Homo sapiens 134-138 24766194-8 2014 The myeloma cells exposed to ASA treatment displayed concentration-dependent apoptosis, which was closely associated with activation of caspases, upregulation of Bax, and downregulation of Bcl-2 and VEGF. Aspirin 29-32 vascular endothelial growth factor A Homo sapiens 199-203 24127927-2 2013 We undertook a prospective study to determine the influence of a 45-day course of aspirin therapy on circulating and intraplatelet levels of selected proangiogenic (vascular endothelial growth factor [VEGF]) and antiangiogenic (thrombospondin-1 [TSP-1]) proteins, and platelet protein release in women diagnosed with breast cancer who were receiving tamoxifen therapy. Aspirin 82-89 vascular endothelial growth factor A Homo sapiens 201-205 24127927-4 2013 Following aspirin therapy, VEGF levels decreased (relative to pretreatment levels) while TSP-1 returned to pretreatment levels. Aspirin 10-17 vascular endothelial growth factor A Homo sapiens 27-31 24127927-6 2013 Aspirin use also decreased thrombin receptor mediated release of TSP-1 and VEGF from platelets. Aspirin 0-7 vascular endothelial growth factor A Homo sapiens 75-79 22431874-0 2012 Vascular endothelial growth factor expression in nasal polyps of aspirin-intolerant patients. Aspirin 65-72 vascular endothelial growth factor A Homo sapiens 0-34 22431874-1 2012 OBJECTIVE: To study differences between aspirin-tolerant patients and aspirin-intolerant patients concerning vascular endothelial growth factor (VEGF) expression. Aspirin 40-47 vascular endothelial growth factor A Homo sapiens 109-143 22431874-1 2012 OBJECTIVE: To study differences between aspirin-tolerant patients and aspirin-intolerant patients concerning vascular endothelial growth factor (VEGF) expression. Aspirin 40-47 vascular endothelial growth factor A Homo sapiens 145-149 22431874-1 2012 OBJECTIVE: To study differences between aspirin-tolerant patients and aspirin-intolerant patients concerning vascular endothelial growth factor (VEGF) expression. Aspirin 70-77 vascular endothelial growth factor A Homo sapiens 109-143 22431874-1 2012 OBJECTIVE: To study differences between aspirin-tolerant patients and aspirin-intolerant patients concerning vascular endothelial growth factor (VEGF) expression. Aspirin 70-77 vascular endothelial growth factor A Homo sapiens 145-149 22431874-10 2012 RESULTS: We found higher expressed levels of VEGF and neuropilin and stronger proliferation in nasal polyps from aspirin-tolerant and aspirin-intolerant patients compared with controls. Aspirin 113-120 vascular endothelial growth factor A Homo sapiens 45-49 22431874-10 2012 RESULTS: We found higher expressed levels of VEGF and neuropilin and stronger proliferation in nasal polyps from aspirin-tolerant and aspirin-intolerant patients compared with controls. Aspirin 134-141 vascular endothelial growth factor A Homo sapiens 45-49 22431874-11 2012 In polyps from aspirin-intolerant patients, VEGF was expressed at considerably higher levels compared with those from aspirin-tolerant subjects. Aspirin 15-22 vascular endothelial growth factor A Homo sapiens 44-48 22431874-13 2012 CONCLUSIONS: Nasal polyps from aspirin-tolerant and aspirin-intolerant patients are characterized by strong proliferation and high levels of VEGF and neuropilin expression. Aspirin 31-38 vascular endothelial growth factor A Homo sapiens 141-145 22431874-13 2012 CONCLUSIONS: Nasal polyps from aspirin-tolerant and aspirin-intolerant patients are characterized by strong proliferation and high levels of VEGF and neuropilin expression. Aspirin 52-59 vascular endothelial growth factor A Homo sapiens 141-145 22431874-14 2012 Nasal polyps from aspirin-intolerant patients show distinctly increased VEGF levels. Aspirin 18-25 vascular endothelial growth factor A Homo sapiens 72-76 22240749-6 2012 Pretreatment with ASA and salicylic acid prevented changes in adherence junction proteins and inhibited VEGF-induced tube formation by HUVECs in a dose-dependent manner. Aspirin 18-21 vascular endothelial growth factor A Homo sapiens 104-108 21330458-14 2011 Activation of VEGF and coagulation (vWF) pathways could partially explain at a molecular level the clinical observations that bevacizumab and aspirin have a preventive effect in SOS. Aspirin 142-149 vascular endothelial growth factor A Homo sapiens 14-18