PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 28583479-1 2018 BACKGROUND: The pathogenesis of aspirin-exacerbated respiratory disease (AERD) is characterized by the low expression of cyclooxygenase-2 (COX-2) in airway epithelia, which decreases the production of prostaglandin E2 (PGE2). Aspirin 32-39 prostaglandin-endoperoxide synthase 2 Homo sapiens 121-137 28583479-1 2018 BACKGROUND: The pathogenesis of aspirin-exacerbated respiratory disease (AERD) is characterized by the low expression of cyclooxygenase-2 (COX-2) in airway epithelia, which decreases the production of prostaglandin E2 (PGE2). Aspirin 32-39 prostaglandin-endoperoxide synthase 2 Homo sapiens 139-144 28528204-6 2017 Moreover, aspirin differentially regulated the expression of a number of inflammation-related genes as it downregulated such pro-inflammatory genes as Nos2, Kng1, IL1beta, Ptgs2 or Ccr1, while it upregulated some anti-inflammatory genes such as IL10, Csf2, Cxcl1, Ccl5 or Tgfb1. Aspirin 10-17 prostaglandin-endoperoxide synthase 2 Homo sapiens 172-177 29149707-0 2017 Over-expression of cyclooxygenase-2 in increased reticulated platelets leads to aspirin resistance after elective off-pump coronary artery bypass surgery. Aspirin 80-87 prostaglandin-endoperoxide synthase 2 Homo sapiens 19-35 28410791-2 2017 We hypothesised that a cyclooxygenase-2-selective NSAID plus proton-pump inhibitor is superior to a non-selective NSAID plus proton-pump inhibitor for prevention of recurrent ulcer bleeding in concomitant users of aspirin with previous ulcer bleeding. Aspirin 214-221 prostaglandin-endoperoxide synthase 2 Homo sapiens 23-39 29087320-8 2017 Inhibition of NOS2 and COX2 using amino-guanidine and aspirin/indomethacin yielded an additive reduction in the growth of MDA-MB-231 tumor xenografts. Aspirin 54-61 prostaglandin-endoperoxide synthase 2 Homo sapiens 23-27 28713783-7 2017 Aspirin, a cyclooxygenase 2 inhibitor, prevented the adhesion of THP-1 cells to HUVECs and did not induce ICAM1 and VCAM1 expression in HUVECs treated with SlaA. Aspirin 0-7 prostaglandin-endoperoxide synthase 2 Homo sapiens 11-27 28285696-5 2017 The lack of survival benefit in patients with small-cell lung cancer taking long-term aspirin may be due to the low expression of cyclooxygenase-2 in small-cell lung cancer tissue. Aspirin 86-93 prostaglandin-endoperoxide synthase 2 Homo sapiens 130-146 28579807-13 2017 Since cyclooxygenase-2 (COX-2) inhibitors (eg, celecoxib) are associated with important cardiovascular events and gastrointestinal harms, more attention is warranted toward CPAs with a favorable benefit-to-risk ratio, such as low-dose aspirin and calcium. Aspirin 235-242 prostaglandin-endoperoxide synthase 2 Homo sapiens 24-29 28448072-1 2017 OBJECTIVES: The association between aspirin use and improved survival after colorectal cancer diagnosis may be more pronounced in tumors that have PIK3CA mutations or high PTGS2 expression. Aspirin 36-43 prostaglandin-endoperoxide synthase 2 Homo sapiens 172-177 28448072-10 2017 The aspirin by PTGS2 interaction was significant for overall survival (PTGS2-high adjusted HR=0.64, 95% CI 0.42-0.98 vs. PTGS2-low adjusted HR=1.28, 95% CI 0.80-2.03, P for interaction=0.04). Aspirin 4-11 prostaglandin-endoperoxide synthase 2 Homo sapiens 15-20 28448072-10 2017 The aspirin by PTGS2 interaction was significant for overall survival (PTGS2-high adjusted HR=0.64, 95% CI 0.42-0.98 vs. PTGS2-low adjusted HR=1.28, 95% CI 0.80-2.03, P for interaction=0.04). Aspirin 4-11 prostaglandin-endoperoxide synthase 2 Homo sapiens 71-76 28448072-10 2017 The aspirin by PTGS2 interaction was significant for overall survival (PTGS2-high adjusted HR=0.64, 95% CI 0.42-0.98 vs. PTGS2-low adjusted HR=1.28, 95% CI 0.80-2.03, P for interaction=0.04). Aspirin 4-11 prostaglandin-endoperoxide synthase 2 Homo sapiens 71-76 28684123-10 2017 On the other hand, higher aspirin doses have been reported to exert a negative impact on blood pressure due to inhibition of cyclooxygenase-2 activity, which reduces renal blood flow, glomerular filtration rate and sodium and water excretion. Aspirin 26-33 prostaglandin-endoperoxide synthase 2 Homo sapiens 125-141 28190074-4 2017 Besides inhibiting the cyclooxygenase 2-prostaglandin axis, ASA"s anti-cancer activities have also been attributed to nuclear factor kB (NFkB) inhibition. Aspirin 60-63 prostaglandin-endoperoxide synthase 2 Homo sapiens 23-39 28107149-0 2016 Release of cyclooxygenase-2 and lipoxin A4 from blood leukocytes in aspirin-exacerbated respiratory disease. Aspirin 68-75 prostaglandin-endoperoxide synthase 2 Homo sapiens 11-27 27565221-4 2016 We have previously reported the preparation of a novel aspirin derivative that we named Ca-Asp, and showed that it causes less damage to gastric mucosa of rat and inhibits the expression of COX-2 to higher degree than Asp. Aspirin 55-62 prostaglandin-endoperoxide synthase 2 Homo sapiens 190-195 26957558-1 2016 PURPOSE: Prostaglandin-endoperoxide synthase 2 (PTGS2, cyclooxygenase-2; a target of aspirin) produces inflammatory mediator prostaglandin E2 (PGE2), and contributes to colorectal neoplasia development. Aspirin 85-92 prostaglandin-endoperoxide synthase 2 Homo sapiens 9-46 26957558-1 2016 PURPOSE: Prostaglandin-endoperoxide synthase 2 (PTGS2, cyclooxygenase-2; a target of aspirin) produces inflammatory mediator prostaglandin E2 (PGE2), and contributes to colorectal neoplasia development. Aspirin 85-92 prostaglandin-endoperoxide synthase 2 Homo sapiens 48-53 26957558-1 2016 PURPOSE: Prostaglandin-endoperoxide synthase 2 (PTGS2, cyclooxygenase-2; a target of aspirin) produces inflammatory mediator prostaglandin E2 (PGE2), and contributes to colorectal neoplasia development. Aspirin 85-92 prostaglandin-endoperoxide synthase 2 Homo sapiens 55-71 26844701-12 2016 Inhibition of COX-2 with aspirin or celecoxib did not affect Caspase-3 levels but also reduced Ki-67 and beta-Catenin levels, suggesting that Caspase-3 acted via COX-2 to stimulate cell proliferation and tissue regeneration. Aspirin 25-32 prostaglandin-endoperoxide synthase 2 Homo sapiens 14-19 27475305-2 2016 Aspirin, a nonsteroidal anti-inflammatory drug, inhibits prostaglandin-endoperoxide synthase 2 (PTGS2 or cyclooxygenase-2); PTGS2 promotes inflammation and suppresses T-cell-mediated adaptive immunity. Aspirin 0-7 prostaglandin-endoperoxide synthase 2 Homo sapiens 57-94 27475305-2 2016 Aspirin, a nonsteroidal anti-inflammatory drug, inhibits prostaglandin-endoperoxide synthase 2 (PTGS2 or cyclooxygenase-2); PTGS2 promotes inflammation and suppresses T-cell-mediated adaptive immunity. Aspirin 0-7 prostaglandin-endoperoxide synthase 2 Homo sapiens 96-101 27475305-2 2016 Aspirin, a nonsteroidal anti-inflammatory drug, inhibits prostaglandin-endoperoxide synthase 2 (PTGS2 or cyclooxygenase-2); PTGS2 promotes inflammation and suppresses T-cell-mediated adaptive immunity. Aspirin 0-7 prostaglandin-endoperoxide synthase 2 Homo sapiens 105-121 27475305-2 2016 Aspirin, a nonsteroidal anti-inflammatory drug, inhibits prostaglandin-endoperoxide synthase 2 (PTGS2 or cyclooxygenase-2); PTGS2 promotes inflammation and suppresses T-cell-mediated adaptive immunity. Aspirin 0-7 prostaglandin-endoperoxide synthase 2 Homo sapiens 124-129 26859324-0 2016 Crystal Structure of Aspirin-Acetylated Human Cyclooxygenase-2: Insight into the Formation of Products with Reversed Stereochemistry. Aspirin 21-28 prostaglandin-endoperoxide synthase 2 Homo sapiens 46-62 28107149-1 2016 BACKGROUND: The release of cyclooxygenase-2 (COX-2) and lipoxin A4 (LXA4) from blood mononuclear cells in patients with aspirin-exacerbated respiratory disease (AERD) is only partially understood. Aspirin 120-127 prostaglandin-endoperoxide synthase 2 Homo sapiens 27-43 28107149-1 2016 BACKGROUND: The release of cyclooxygenase-2 (COX-2) and lipoxin A4 (LXA4) from blood mononuclear cells in patients with aspirin-exacerbated respiratory disease (AERD) is only partially understood. Aspirin 120-127 prostaglandin-endoperoxide synthase 2 Homo sapiens 45-50 26475800-4 2015 Additional cyclooxygenase-2 blockade by high-dose aspirin might decrease the antithrombotic efficacy by inhibiting endothelial prostacyclin synthesis. Aspirin 50-57 prostaglandin-endoperoxide synthase 2 Homo sapiens 11-27 25967073-2 2015 Aspirin is a potent inhibitor of cyclooxygenase-2 (COX), which plays a critical role in the expression of immune modulators known to contribute to cerebral aneurysm formation and rupture. Aspirin 0-7 prostaglandin-endoperoxide synthase 2 Homo sapiens 33-49 25239119-8 2015 Besides, the survival benefit of postdiagnosis aspirin use appeared to be confined to those patients with positive prostaglandin endoperoxide synthase 2 (PTGS2, also known as cyclooxygenase-2, COX-2) expression (HR=0.65, 95% CI 0.50 to 0.85) and with mutated PIK3CA tumours (HR=0.58, 95% CI 0.37 to 0.90). Aspirin 47-54 prostaglandin-endoperoxide synthase 2 Homo sapiens 115-152 25239119-8 2015 Besides, the survival benefit of postdiagnosis aspirin use appeared to be confined to those patients with positive prostaglandin endoperoxide synthase 2 (PTGS2, also known as cyclooxygenase-2, COX-2) expression (HR=0.65, 95% CI 0.50 to 0.85) and with mutated PIK3CA tumours (HR=0.58, 95% CI 0.37 to 0.90). Aspirin 47-54 prostaglandin-endoperoxide synthase 2 Homo sapiens 154-159 25239119-8 2015 Besides, the survival benefit of postdiagnosis aspirin use appeared to be confined to those patients with positive prostaglandin endoperoxide synthase 2 (PTGS2, also known as cyclooxygenase-2, COX-2) expression (HR=0.65, 95% CI 0.50 to 0.85) and with mutated PIK3CA tumours (HR=0.58, 95% CI 0.37 to 0.90). Aspirin 47-54 prostaglandin-endoperoxide synthase 2 Homo sapiens 175-191 25239119-11 2015 CONCLUSIONS: These findings provide further indication that postdiagnosis aspirin therapy improved CRC overall survival, especially for patients with positive PTGS2 (COX-2) expression and mutated PIK3CA tumours. Aspirin 74-81 prostaglandin-endoperoxide synthase 2 Homo sapiens 159-164 25895638-4 2015 ATL biosynthesis requires cyclooxygenase-2 acetylation by aspirin. Aspirin 58-65 prostaglandin-endoperoxide synthase 2 Homo sapiens 26-42 26068794-7 2015 The effects of ASA and BoxA were cyclooxygenase-2 independent and were not additive, consistent with both acting via inhibition of HMGB1 activity. Aspirin 15-18 prostaglandin-endoperoxide synthase 2 Homo sapiens 33-49 25514511-2 2015 The principal pharmacological effects of aspirin are known to arise from its covalent modification of cyclooxygenase-2 (COX-2) through acetylation of Ser530, but the detailed mechanism of its biochemical action and specificity remains to be elucidated. Aspirin 41-48 prostaglandin-endoperoxide synthase 2 Homo sapiens 102-118 25514511-2 2015 The principal pharmacological effects of aspirin are known to arise from its covalent modification of cyclooxygenase-2 (COX-2) through acetylation of Ser530, but the detailed mechanism of its biochemical action and specificity remains to be elucidated. Aspirin 41-48 prostaglandin-endoperoxide synthase 2 Homo sapiens 120-125 25514511-5 2015 The computational results confirmed that aspirin would be 10-100 times more potent against COX-1 than against COX-2, and revealed that this inhibition specificity between the two COX isoforms can be attributed mainly to the difference in kinetics rate of the covalent inhibition reaction, not the aspirin-binding step. Aspirin 41-48 prostaglandin-endoperoxide synthase 2 Homo sapiens 110-115 25012137-10 2014 Adenosine-receptor antagonism blocked the ticagrelor effect and COX2 inhibition by SC5815, or high-dose aspirin attenuated the IS-limiting effect of ticagrelor, whereas cyclooxygenase-1 inhibition or low-dose aspirin had no effect. Aspirin 104-111 prostaglandin-endoperoxide synthase 2 Homo sapiens 64-68 25368225-3 2014 Drugs with the ability to inhibit COX-2 expression include aspirin, nonsteroidal anti-inflammatory drugs (NSAID) and selective COX-2 inhibitors. Aspirin 59-66 prostaglandin-endoperoxide synthase 2 Homo sapiens 34-39 25139986-6 2014 Initial activation of TLR4 results in accumulation of the cyclooxygenase-2-derived lipoxin precursor 15-hydroxyeicosatetraenoic acid (15-HETE) in esterified form within membrane phospholipids, which can be enhanced by aspirin (ASA) treatment. Aspirin 218-225 prostaglandin-endoperoxide synthase 2 Homo sapiens 58-74 25139986-6 2014 Initial activation of TLR4 results in accumulation of the cyclooxygenase-2-derived lipoxin precursor 15-hydroxyeicosatetraenoic acid (15-HETE) in esterified form within membrane phospholipids, which can be enhanced by aspirin (ASA) treatment. Aspirin 227-230 prostaglandin-endoperoxide synthase 2 Homo sapiens 58-74 24958470-7 2014 Interestingly, cyclooxygenase-2 inhibition by aspirin or celecoxib abrogated IL-1beta-mediated repression of miR-101 and IL-1beta-mediated activation of Lin28B along with their stimulatory effects on NSCLC cell proliferation and migration. Aspirin 46-53 prostaglandin-endoperoxide synthase 2 Homo sapiens 15-31 24760190-1 2014 Aspirin use reduces the risk of colorectal neoplasia, at least in part, through inhibition of prostaglandin-endoperoxide synthase 2 (PTGS2, cyclooxygenase 2)-related pathways. Aspirin 0-7 prostaglandin-endoperoxide synthase 2 Homo sapiens 94-131 24908358-2 2014 Direct inhibition of cyclooxygenase-2 (COX-2) pathway is generally thought to be the main mechanism by which aspirin inhibits cancer development. Aspirin 109-116 prostaglandin-endoperoxide synthase 2 Homo sapiens 21-37 24908358-2 2014 Direct inhibition of cyclooxygenase-2 (COX-2) pathway is generally thought to be the main mechanism by which aspirin inhibits cancer development. Aspirin 109-116 prostaglandin-endoperoxide synthase 2 Homo sapiens 39-44 24687028-10 2014 The benefit of aspirin was similar for tumors with strong PTGS2 expression (0.68; 0.48-0.97; P = .03), weak PTGS2 expression (0.59; 0.38-0.97; P = .02), and wild-type PIK3CA tumors (0.55; 0.40-0.75; P < .001). Aspirin 15-22 prostaglandin-endoperoxide synthase 2 Homo sapiens 58-63 24760190-1 2014 Aspirin use reduces the risk of colorectal neoplasia, at least in part, through inhibition of prostaglandin-endoperoxide synthase 2 (PTGS2, cyclooxygenase 2)-related pathways. Aspirin 0-7 prostaglandin-endoperoxide synthase 2 Homo sapiens 133-138 24760190-1 2014 Aspirin use reduces the risk of colorectal neoplasia, at least in part, through inhibition of prostaglandin-endoperoxide synthase 2 (PTGS2, cyclooxygenase 2)-related pathways. Aspirin 0-7 prostaglandin-endoperoxide synthase 2 Homo sapiens 140-156 24708725-1 2014 INTRODUCTION: Recent observational studies indicate that post-diagnostic use of aspirin in breast cancer patients may protect against cancer progression perhaps by inhibiting cyclooxygenase-2 dependent mechanisms. Aspirin 80-87 prostaglandin-endoperoxide synthase 2 Homo sapiens 175-191 24395886-10 2014 15-epi-lipoxin-A4 was identified in exhaled breath condensate from LAM subjects and was increased by aspirin treatment, indicative of functional COX-2 expression in the LAM airway. Aspirin 101-108 prostaglandin-endoperoxide synthase 2 Homo sapiens 145-150 24565956-8 2014 In an exploratory analysis, we found that among individuals with high plasma MIC-1 levels (quintiles 2-5), compared with nonuse, regular use of aspirin and nonsteroidal anti-inflammatory drugs (NSAIDs) was associated with a lower risk of PTGS2-positive CRC (multivariable RR = 0.60; 95% confidence interval = 0.41 to 0.88) but not PTGS2-negative CRC (multivariable RR = 1.21; 95% CI = 0.71 to 2.07). Aspirin 144-151 prostaglandin-endoperoxide synthase 2 Homo sapiens 238-243 24565956-8 2014 In an exploratory analysis, we found that among individuals with high plasma MIC-1 levels (quintiles 2-5), compared with nonuse, regular use of aspirin and nonsteroidal anti-inflammatory drugs (NSAIDs) was associated with a lower risk of PTGS2-positive CRC (multivariable RR = 0.60; 95% confidence interval = 0.41 to 0.88) but not PTGS2-negative CRC (multivariable RR = 1.21; 95% CI = 0.71 to 2.07). Aspirin 144-151 prostaglandin-endoperoxide synthase 2 Homo sapiens 331-336 23884755-5 2013 Moreover, use of low-dose aspirin for cardioprotection (a common co-treatment with the selective cyclooxygenase-2 inhibitors) further augments intestinal damage, particularly when enteric-coated aspirin is used. Aspirin 26-33 prostaglandin-endoperoxide synthase 2 Homo sapiens 97-113 25612650-2 2014 The production of lipoxins is enhanced by aspirin through acetylation of cyclooxygenase-2, via a mechanism known as "aspirin-triggered lipoxin". Aspirin 42-49 prostaglandin-endoperoxide synthase 2 Homo sapiens 73-89 25612650-2 2014 The production of lipoxins is enhanced by aspirin through acetylation of cyclooxygenase-2, via a mechanism known as "aspirin-triggered lipoxin". Aspirin 117-124 prostaglandin-endoperoxide synthase 2 Homo sapiens 73-89 23884755-5 2013 Moreover, use of low-dose aspirin for cardioprotection (a common co-treatment with the selective cyclooxygenase-2 inhibitors) further augments intestinal damage, particularly when enteric-coated aspirin is used. Aspirin 195-202 prostaglandin-endoperoxide synthase 2 Homo sapiens 97-113 23434193-5 2013 We also highlight that formation of pro-resolving mediators can be enhanced by widely used anti-inflammatory and cardioprotective drugs (aspirin and statins) via the modification of cyclooxygenase-2 enzymatic activity. Aspirin 137-144 prostaglandin-endoperoxide synthase 2 Homo sapiens 182-198 23955344-9 2013 With or without heme, aspirin acetylates one-half of the subunits of the native PGHS-2 dimer, the Ecat subunits. Aspirin 22-29 prostaglandin-endoperoxide synthase 2 Homo sapiens 80-86 23955344-11 2013 Curiously, aspirin acetylates only one-quarter of the monomers of S530A/Native PGHS-2 with or without heme. Aspirin 11-18 prostaglandin-endoperoxide synthase 2 Homo sapiens 79-85 24098505-6 2013 Further mechanistic studies revealed that the actions of these phytochemicals were similar to aspirin in that they mainly inhibited COX-1 rather than COX-2, especially at low doses. Aspirin 94-101 prostaglandin-endoperoxide synthase 2 Homo sapiens 150-155 23786234-0 2013 A mechanistic hypothesis for the aspirin-induced switch in lipid mediator production by cyclooxygenase-2. Aspirin 33-40 prostaglandin-endoperoxide synthase 2 Homo sapiens 88-104 23810915-1 2013 BACKGROUND: Studies have examined whether tumor expression of PTGS2 (also known as COX-2), an enzyme inhibited by nonsteroidal anti-inflammatory drugs such as aspirin, is associated with prognosis in patients with colorectal cancer. Aspirin 159-166 prostaglandin-endoperoxide synthase 2 Homo sapiens 62-67 23800934-2 2013 Experimental evidence implicates a role of RAF kinases in up-regulation of prostaglandin-endoperoxide synthase 2 (PTGS2, cyclooxygenase 2), suggesting that BRAF-mutant colonic cells might be less sensitive to the antitumor effects of aspirin than BRAF-wild-type neoplastic cells. Aspirin 234-241 prostaglandin-endoperoxide synthase 2 Homo sapiens 75-112 23800934-2 2013 Experimental evidence implicates a role of RAF kinases in up-regulation of prostaglandin-endoperoxide synthase 2 (PTGS2, cyclooxygenase 2), suggesting that BRAF-mutant colonic cells might be less sensitive to the antitumor effects of aspirin than BRAF-wild-type neoplastic cells. Aspirin 234-241 prostaglandin-endoperoxide synthase 2 Homo sapiens 114-119 22763923-0 2013 Association of COX-2 rs20417 with aspirin resistance. Aspirin 34-41 prostaglandin-endoperoxide synthase 2 Homo sapiens 15-20 23200247-1 2013 The observation that the cyclooxygenase-2 (COX-2) isozyme is over-expressed in multiple types of cancer, relative to that in adjacent non-cancerous tissue, prompted this investigation to prepare a group of hybrid fluorescent conjugates wherein the COX inhibitors ibuprofen, (S)-naproxen, acetyl salicylic acid, a chlororofecoxib analog and celecoxib were coupled via a linker group to an acridone, dansyl or rhodamine B fluorophore. Aspirin 288-309 prostaglandin-endoperoxide synthase 2 Homo sapiens 25-41 23200247-1 2013 The observation that the cyclooxygenase-2 (COX-2) isozyme is over-expressed in multiple types of cancer, relative to that in adjacent non-cancerous tissue, prompted this investigation to prepare a group of hybrid fluorescent conjugates wherein the COX inhibitors ibuprofen, (S)-naproxen, acetyl salicylic acid, a chlororofecoxib analog and celecoxib were coupled via a linker group to an acridone, dansyl or rhodamine B fluorophore. Aspirin 288-309 prostaglandin-endoperoxide synthase 2 Homo sapiens 43-48 22588264-13 2012 We speculate that the protective effect of aspirin against rupture of cerebral aneurysms may be mediated in part by inhibition of COX-2/mPGES-1. Aspirin 43-50 prostaglandin-endoperoxide synthase 2 Homo sapiens 130-135 23094721-2 2012 Experimental evidence suggests that inhibition of prostaglandin-endoperoxide synthase 2 (PTGS2) (also known as cyclooxygenase-2) by aspirin down-regulates phosphatidylinositol 3-kinase (PI3K) signaling activity. Aspirin 132-139 prostaglandin-endoperoxide synthase 2 Homo sapiens 50-87 23094721-2 2012 Experimental evidence suggests that inhibition of prostaglandin-endoperoxide synthase 2 (PTGS2) (also known as cyclooxygenase-2) by aspirin down-regulates phosphatidylinositol 3-kinase (PI3K) signaling activity. Aspirin 132-139 prostaglandin-endoperoxide synthase 2 Homo sapiens 89-94 23094721-2 2012 Experimental evidence suggests that inhibition of prostaglandin-endoperoxide synthase 2 (PTGS2) (also known as cyclooxygenase-2) by aspirin down-regulates phosphatidylinositol 3-kinase (PI3K) signaling activity. Aspirin 132-139 prostaglandin-endoperoxide synthase 2 Homo sapiens 111-127 22252409-7 2012 Decreased risks were found among women who used aspirin continuously (0.71 [0.54-0.94]) or at a low-standardized daily dose (0.72 [0.53-0.97]), who used aspirin for the prevention of cardiovascular disease (0.72 [0.57-0.97]), who used aspirin more recently, or who used selective cyclooxygenase-2 inhibitors (0.60 [0.39-0.94]). Aspirin 48-55 prostaglandin-endoperoxide synthase 2 Homo sapiens 280-296 22245433-4 2012 In this study, Asn(580) was mutated, and the mutant and wild-type COX-2 genes were expressed in COS-1 cells to determine how glycosylation affects the inhibition of COX-2 activity by aspirin, flurbiprofen, ibuprofen, celecoxib, and etoricoxib. Aspirin 183-190 prostaglandin-endoperoxide synthase 2 Homo sapiens 165-170 22252409-7 2012 Decreased risks were found among women who used aspirin continuously (0.71 [0.54-0.94]) or at a low-standardized daily dose (0.72 [0.53-0.97]), who used aspirin for the prevention of cardiovascular disease (0.72 [0.57-0.97]), who used aspirin more recently, or who used selective cyclooxygenase-2 inhibitors (0.60 [0.39-0.94]). Aspirin 153-160 prostaglandin-endoperoxide synthase 2 Homo sapiens 280-296 22252409-7 2012 Decreased risks were found among women who used aspirin continuously (0.71 [0.54-0.94]) or at a low-standardized daily dose (0.72 [0.53-0.97]), who used aspirin for the prevention of cardiovascular disease (0.72 [0.57-0.97]), who used aspirin more recently, or who used selective cyclooxygenase-2 inhibitors (0.60 [0.39-0.94]). Aspirin 153-160 prostaglandin-endoperoxide synthase 2 Homo sapiens 280-296 21435744-4 2011 These data support the use of acetylsalicylic acid (AAS) or aspirin, a COX-2 inhibitor, as an effective agent in colorectal cancer prevention. Aspirin 60-67 prostaglandin-endoperoxide synthase 2 Homo sapiens 71-76 23240010-0 2012 Signal transduction pathways (MAPKs, NF-kappaB, and C/EBP) regulating COX-2 expression in nasal fibroblasts from asthma patients with aspirin intolerance. Aspirin 134-141 prostaglandin-endoperoxide synthase 2 Homo sapiens 70-75 23240010-1 2012 BACKGROUND: Recent studies have revealed that cyclooxygenase-2 (COX-2) expression is down-regulated in aspirin-induced asthma (AIA). Aspirin 103-110 prostaglandin-endoperoxide synthase 2 Homo sapiens 46-62 23240010-1 2012 BACKGROUND: Recent studies have revealed that cyclooxygenase-2 (COX-2) expression is down-regulated in aspirin-induced asthma (AIA). Aspirin 103-110 prostaglandin-endoperoxide synthase 2 Homo sapiens 64-69 23240010-3 2012 OBJECTIVE: To investigate the regulation of COX-2 expression through MAP-kinase pathway activation and nuclear factor translocation in aspirin-induced asthma (AIA). Aspirin 135-142 prostaglandin-endoperoxide synthase 2 Homo sapiens 44-49 21728052-2 2011 Aspirin and NSAIDs inhibit COX-2. Aspirin 0-7 prostaglandin-endoperoxide synthase 2 Homo sapiens 27-32 21728052-13 2011 The RR(95% CI) of breast cancer death for current aspirin use was similar for women with COX-2-positive and COX-2-negative tumors; 0.64 (0.43-0.96) and 0.57 (0.44-0.74), respectively. Aspirin 50-57 prostaglandin-endoperoxide synthase 2 Homo sapiens 89-94 21728052-13 2011 The RR(95% CI) of breast cancer death for current aspirin use was similar for women with COX-2-positive and COX-2-negative tumors; 0.64 (0.43-0.96) and 0.57 (0.44-0.74), respectively. Aspirin 50-57 prostaglandin-endoperoxide synthase 2 Homo sapiens 108-113 21728052-17 2011 If aspirin truly impacts breast cancer survival, then it is not solely via COX-2. Aspirin 3-10 prostaglandin-endoperoxide synthase 2 Homo sapiens 75-80 21647198-4 2011 The risk of upper gastrointestinal bleeding with aspirin is increased with old age, male sex, ulcer history and concomitant medication with NSAIDs, cyclooxygenase 2 selective inhibitors, corticosteroids or other antithrombotic agents. Aspirin 49-56 prostaglandin-endoperoxide synthase 2 Homo sapiens 148-164 21703104-0 2011 Selective cyclooxygenase-2 inhibitor cross-reactivity in aspirin-exacerbated respiratory disease. Aspirin 57-64 prostaglandin-endoperoxide synthase 2 Homo sapiens 10-26 22095955-0 2012 Aspirin analogues as dual cyclooxygenase-2/5-lipoxygenase inhibitors: synthesis, nitric oxide release, molecular modeling, and biological evaluation as anti-inflammatory agents. Aspirin 0-7 prostaglandin-endoperoxide synthase 2 Homo sapiens 26-42 22429367-10 2012 CONCLUSIONS: TEG-AA was more sensitive, specific and consistent than the P-selectin assay for detecting aspirin resistance, and the PTGS2 G765C mutation may be related to aspirin resistance. Aspirin 171-178 prostaglandin-endoperoxide synthase 2 Homo sapiens 132-137 21163909-7 2011 Acetylsalicylic acid, an irreversible inhibitor of both hPHS-1 and hPHS-2, blocked cytotoxicity and DNA oxidation in both cell lines and untransfected CHO-K1 cells lacking PHS activity were similarly resistant. Aspirin 0-20 prostaglandin-endoperoxide synthase 2 Homo sapiens 67-73 20864907-11 2010 Following appropriate discussions, acetylsalicylic acid (ASA) can soon be restarted acutely after bleeding; long-term PPI co-therapy is imperative in patients having bled on nonsteroidal anti-inflammatory drugs if still needed (preferably with a cyclooxygenase-2, if appropriate) or ASA (not clopidogrel alone). Aspirin 57-60 prostaglandin-endoperoxide synthase 2 Homo sapiens 246-262 21331307-0 2010 COX-2 Inhibition by Use of Rofecoxib or High Dose Aspirin Enhances ADP-Induced Platelet Aggregation in Fresh Blood. Aspirin 50-57 prostaglandin-endoperoxide synthase 2 Homo sapiens 0-5 20697066-8 2010 Use of aspirin is proven to lower risk of colorectal cancer, and recent evidence suggests that aspirin use in patients with colorectal cancer improves cancer-specific and overall survival, especially in patients with tumors that express cyclooxygenase-2 (COX-2). Aspirin 95-102 prostaglandin-endoperoxide synthase 2 Homo sapiens 237-253 20697066-8 2010 Use of aspirin is proven to lower risk of colorectal cancer, and recent evidence suggests that aspirin use in patients with colorectal cancer improves cancer-specific and overall survival, especially in patients with tumors that express cyclooxygenase-2 (COX-2). Aspirin 95-102 prostaglandin-endoperoxide synthase 2 Homo sapiens 255-260 20665602-5 2010 The results showed that after the endothelial cells were incubated with 250 muM of hydrogen peroxide for 12 h, apoptosis increased, which was antagonized by the cyclooxygenase-2 inhibitor nimesulide or the nonselective cyclooxygenase inhibitor aspirin, but not by the cyclooxygenase-1 inhibitor piroxicam. Aspirin 244-251 prostaglandin-endoperoxide synthase 2 Homo sapiens 161-177 20397022-1 2010 PURPOSE: To investigate the effect of cyclooxygenase-2 (Cox-2) inhibitor aspirin (acetylsalicylic acid, ASA) and proteasome inhibitor bortezomib in the proliferation and apoptosis of colorectal cancer cell lines. Aspirin 73-80 prostaglandin-endoperoxide synthase 2 Homo sapiens 38-54 22396856-9 2010 This depends on the allosteric effects of ASA on cyclooxygenase-2 and following production - from DHA - of specific lipid mediators (resolvins, protectins, and electrophilic oxo-derivatives). Aspirin 42-45 prostaglandin-endoperoxide synthase 2 Homo sapiens 49-65 20397022-1 2010 PURPOSE: To investigate the effect of cyclooxygenase-2 (Cox-2) inhibitor aspirin (acetylsalicylic acid, ASA) and proteasome inhibitor bortezomib in the proliferation and apoptosis of colorectal cancer cell lines. Aspirin 73-80 prostaglandin-endoperoxide synthase 2 Homo sapiens 56-61 20397022-1 2010 PURPOSE: To investigate the effect of cyclooxygenase-2 (Cox-2) inhibitor aspirin (acetylsalicylic acid, ASA) and proteasome inhibitor bortezomib in the proliferation and apoptosis of colorectal cancer cell lines. Aspirin 82-102 prostaglandin-endoperoxide synthase 2 Homo sapiens 56-61 20397022-6 2010 In the first two cell lines ASA inhibitory effects are Cox-2 independent because HCT116 cells do not express the enzyme while in HT-29 cells, Cox-2 has no activity as shown by a Cox activity assay. Aspirin 28-31 prostaglandin-endoperoxide synthase 2 Homo sapiens 55-60 20397022-7 2010 In CaCo2 cells that express enzymatically active Cox-2 this activity is inhibited by ASA. Aspirin 85-88 prostaglandin-endoperoxide synthase 2 Homo sapiens 49-54 20397022-8 2010 ASA is also able to suppress the increase in Cox-2 activity induced by bortezomib in these cells. Aspirin 0-3 prostaglandin-endoperoxide synthase 2 Homo sapiens 45-50 20194532-0 2010 Asymmetric acetylation of the cyclooxygenase-2 homodimer by aspirin and its effects on the oxygenation of arachidonic, eicosapentaenoic, and docosahexaenoic acids. Aspirin 60-67 prostaglandin-endoperoxide synthase 2 Homo sapiens 30-46 20436486-4 2010 Modulation of COX-2 activity by aspirin increased the rate of EFOX production and their intracellular levels. Aspirin 32-39 prostaglandin-endoperoxide synthase 2 Homo sapiens 14-19 20194532-3 2010 Here we report that aspirin maximally acetylates one monomer of human (hu) PGHS-2. Aspirin 20-27 prostaglandin-endoperoxide synthase 2 Homo sapiens 75-81 20194532-6 2010 The 18R- and 17R-resolvins putatively involved in resolution of inflammation are reportedly formed via aspirin-acetylated PGHS-2 from eicosapentaenoic acid and docosahexaenoic acid, respectively, so we also characterized the oxygenation of these omega-3 fatty acids by aspirin-treated huPGHS-2. Aspirin 103-110 prostaglandin-endoperoxide synthase 2 Homo sapiens 122-128 20194532-6 2010 The 18R- and 17R-resolvins putatively involved in resolution of inflammation are reportedly formed via aspirin-acetylated PGHS-2 from eicosapentaenoic acid and docosahexaenoic acid, respectively, so we also characterized the oxygenation of these omega-3 fatty acids by aspirin-treated huPGHS-2. Aspirin 269-276 prostaglandin-endoperoxide synthase 2 Homo sapiens 122-128 19887674-1 2010 We tested whether cyclooxygenase 2 (COX-2) expression and unacetylated COX-1 in newly formed platelets might contribute to persistent thromboxane (TX) biosynthesis in aspirin-treated essential thrombocythemia (ET). Aspirin 167-174 prostaglandin-endoperoxide synthase 2 Homo sapiens 18-34 20427397-10 2010 The protective effect of aspirin was mainly observed in patients in whom COX-2 initial expression was low (RR for recurrence in patients taking aspirin with low COX-2 expression: 0.59; 95% CI 0.39 to 0.90; p=0.02). Aspirin 25-32 prostaglandin-endoperoxide synthase 2 Homo sapiens 73-78 20427397-10 2010 The protective effect of aspirin was mainly observed in patients in whom COX-2 initial expression was low (RR for recurrence in patients taking aspirin with low COX-2 expression: 0.59; 95% CI 0.39 to 0.90; p=0.02). Aspirin 25-32 prostaglandin-endoperoxide synthase 2 Homo sapiens 161-166 20427397-10 2010 The protective effect of aspirin was mainly observed in patients in whom COX-2 initial expression was low (RR for recurrence in patients taking aspirin with low COX-2 expression: 0.59; 95% CI 0.39 to 0.90; p=0.02). Aspirin 144-151 prostaglandin-endoperoxide synthase 2 Homo sapiens 161-166 19633925-5 2010 In addition, the combination treatment of COX-2 siRNA and acidum acetil salicylicum (aspirin) has a synergistic effect. Aspirin 85-92 prostaglandin-endoperoxide synthase 2 Homo sapiens 42-47 19887674-10 2010 Accelerated platelet regeneration in most aspirin-treated ET patients may explain aspirin-persistent TXA(2) biosynthesis through enhanced COX-2 activity and faster renewal of unacetylated COX-1. Aspirin 82-89 prostaglandin-endoperoxide synthase 2 Homo sapiens 138-143 19887674-1 2010 We tested whether cyclooxygenase 2 (COX-2) expression and unacetylated COX-1 in newly formed platelets might contribute to persistent thromboxane (TX) biosynthesis in aspirin-treated essential thrombocythemia (ET). Aspirin 167-174 prostaglandin-endoperoxide synthase 2 Homo sapiens 36-41 19887674-10 2010 Accelerated platelet regeneration in most aspirin-treated ET patients may explain aspirin-persistent TXA(2) biosynthesis through enhanced COX-2 activity and faster renewal of unacetylated COX-1. Aspirin 42-49 prostaglandin-endoperoxide synthase 2 Homo sapiens 138-143 19755647-3 2009 Aspirin inhibits COX-2 activity and lowers the risk for colorectal adenomas and cancer. Aspirin 0-7 prostaglandin-endoperoxide synthase 2 Homo sapiens 17-22 19755647-10 2009 These results support the hypothesis that COX-2 plays a role in the etiology of colon cancer and may be a target for aspirin chemoprevention and warrant further investigation in other colorectal adenoma and cancer populations. Aspirin 117-124 prostaglandin-endoperoxide synthase 2 Homo sapiens 42-47 18373616-3 2008 Aspirin, non-steroidal anti-inflammatory drugs (NSAIDs) and cyclooxygenase 2 (Cox-2) inhibitors have been shown to decrease the incidence of colorectal cancer. Aspirin 0-7 prostaglandin-endoperoxide synthase 2 Homo sapiens 78-83 19671906-10 2009 Among 459 participants with colorectal cancers that were accessible for immunohistochemical assessment, the effect of aspirin differed significantly according to cyclooxygenase 2 (COX-2) expression (P for interaction = .04). Aspirin 118-125 prostaglandin-endoperoxide synthase 2 Homo sapiens 162-178 19671906-10 2009 Among 459 participants with colorectal cancers that were accessible for immunohistochemical assessment, the effect of aspirin differed significantly according to cyclooxygenase 2 (COX-2) expression (P for interaction = .04). Aspirin 118-125 prostaglandin-endoperoxide synthase 2 Homo sapiens 180-185 19671906-11 2009 Regular aspirin use after diagnosis was associated with a lower risk of colorectal cancer-specific mortality among participants in whom primary tumors overexpressed COX-2 (multivariate HR, 0.39; 95% CI, 0.20-0.76), whereas aspirin use was not associated with lower risk among those with primary tumors with weak or absent expression (multivariate HR, 1.22; 95% CI, 0.36-4.18). Aspirin 8-15 prostaglandin-endoperoxide synthase 2 Homo sapiens 165-170 19671906-12 2009 CONCLUSION: Regular aspirin use after the diagnosis of colorectal cancer is associated with lower risk of colorectal cancer-specific and overall mortality, especially among individuals with tumors that overexpress COX-2. Aspirin 20-27 prostaglandin-endoperoxide synthase 2 Homo sapiens 214-219 19306941-4 2009 In this evidence-based review, we have endeavored to answer 12 commonly encountered questions in clinical practice that deal with the following: extent of the problem of NSAID/aspirin-induced gastroduodenal damage and its impact on public health; role of proton pump inhibitors (PPIs) in the primary prevention, healing, and secondary prevention of NSAID/aspirin-induced gastroduodenal ulceration as assessed by using endoscopic end points; role of PPIs in the prevention of adverse clinical outcomes related to NSAID/aspirin use; whether PPIs are effective in NSAID-induced dyspepsia; comparison of PPI co-therapy with selective cyclooxygenase-2 inhibitors for risk reduction of adverse clinical outcomes; role of PPIs in preventing rebleeding from aspirin +/- clopidogrel therapy in high-risk patients; identifying high-risk patients who can benefit from PPI co-therapy; the role of other gastroprotective agents for prevention of NSAID/aspirin-induced gastroduodenal damage; and the cost-effectiveness of and limitations to the use of PPIs for prevention of gastroduodenal damage related to the use of NSAIDs or aspirin. Aspirin 176-183 prostaglandin-endoperoxide synthase 2 Homo sapiens 630-646 19046748-3 2009 A secondary aim was to replicate the interaction of PTGS2 rs20417 (-765G to C) with aspirin use on coronary heart disease risk observed in the Atherosclerosis Risk in Communities Study (ARIC). Aspirin 84-91 prostaglandin-endoperoxide synthase 2 Homo sapiens 52-57 19299662-3 2009 Indeed, a new class of selective inhibitors of the cyclooxygenase-2 isozyme was introduced, about ten years ago, and these so-called coxibs quickly became regarded as preferable, in certain clinical contexts, to avoid side effects associated with the use of aspirin and previously developed NSAIDs. Aspirin 258-265 prostaglandin-endoperoxide synthase 2 Homo sapiens 51-67 19026633-3 2009 Furthermore, we demonstrated that the non-steroidal anti-inflammatory drug, sulindac sulfide, the cyclooxygenase-2 (COX-2) selective inhibitor, celecoxib, and the nitric oxide-donating aspirin derivative, NO-ASA, blocked Wnt/beta-catenin signaling in PC-3 and DU145 cells. Aspirin 185-192 prostaglandin-endoperoxide synthase 2 Homo sapiens 116-121 19026633-3 2009 Furthermore, we demonstrated that the non-steroidal anti-inflammatory drug, sulindac sulfide, the cyclooxygenase-2 (COX-2) selective inhibitor, celecoxib, and the nitric oxide-donating aspirin derivative, NO-ASA, blocked Wnt/beta-catenin signaling in PC-3 and DU145 cells. Aspirin 208-211 prostaglandin-endoperoxide synthase 2 Homo sapiens 98-114 19295242-7 2009 CONCLUSIONS: The main finding of this study is that COX-2 appears to be differentially regulated in aspirin-sensitive patients. Aspirin 100-107 prostaglandin-endoperoxide synthase 2 Homo sapiens 52-57 19295242-8 2009 What is really new is the observation that aspirin and LPS increase COX-2 expression on blood monocytes of AI asthmatics, a finding in contrast with the lack of an effect of the same stimuli on COX-2 expression on monocytes from healthy subjects. Aspirin 43-50 prostaglandin-endoperoxide synthase 2 Homo sapiens 68-73 18660649-3 2008 All NSAIDs and aspirin inhibit active sites of cyclooxygenase-1 and cyclooxygenase-2. Aspirin 15-22 prostaglandin-endoperoxide synthase 2 Homo sapiens 68-84 18393288-0 2008 Acetylsalicylic acid inhibits hepatitis C virus RNA and protein expression through cyclooxygenase 2 signaling pathways. Aspirin 0-20 prostaglandin-endoperoxide synthase 2 Homo sapiens 83-99 18393288-7 2008 However, we found that HCV-induced cyclooxygenase 2 (COX-2) messenger RNA and protein levels and activity and these effects were down-regulated by ASA, possibly by a nuclear factor kappa B-independent mechanism. Aspirin 147-150 prostaglandin-endoperoxide synthase 2 Homo sapiens 35-51 18393288-7 2008 However, we found that HCV-induced cyclooxygenase 2 (COX-2) messenger RNA and protein levels and activity and these effects were down-regulated by ASA, possibly by a nuclear factor kappa B-independent mechanism. Aspirin 147-150 prostaglandin-endoperoxide synthase 2 Homo sapiens 53-58 18393288-8 2008 We also observed that the ASA-dependent inhibition of viral replication was due in part to inhibition of COX-2 and activation of p38 and mitogen-activated protein kinase/extracellular signal-regulated kinase kinase 1/2 (MEK1/2) mitogen-activated protein kinases (MAPKs). Aspirin 26-29 prostaglandin-endoperoxide synthase 2 Homo sapiens 105-110 18393288-10 2008 Taken together, our findings suggest that the anti-HCV effect of ASA in the Huh7 replicon cells is due to its inhibitory effect on COX-2 expression, which is mediated in part by the activation of MEK1/2/p38 MAPK. Aspirin 65-68 prostaglandin-endoperoxide synthase 2 Homo sapiens 131-136 19295242-0 2009 Aspirin-induced COX-2 overexpression in monocytes of aspirin-intolerant patients. Aspirin 0-7 prostaglandin-endoperoxide synthase 2 Homo sapiens 16-21 19295242-0 2009 Aspirin-induced COX-2 overexpression in monocytes of aspirin-intolerant patients. Aspirin 53-60 prostaglandin-endoperoxide synthase 2 Homo sapiens 16-21 19295242-1 2009 BACKGROUND: We hypothesize that alternate regulation of cyclooxygenase-2 (COX-2) may predispose patients to aspirin-induced exacerbations.Therefore, we want to examine the dynamics of COX-2 up-regulation in whole blood monocytes in the presence and absence of aspirin. Aspirin 108-115 prostaglandin-endoperoxide synthase 2 Homo sapiens 56-72 19295242-1 2009 BACKGROUND: We hypothesize that alternate regulation of cyclooxygenase-2 (COX-2) may predispose patients to aspirin-induced exacerbations.Therefore, we want to examine the dynamics of COX-2 up-regulation in whole blood monocytes in the presence and absence of aspirin. Aspirin 108-115 prostaglandin-endoperoxide synthase 2 Homo sapiens 74-79 19295242-1 2009 BACKGROUND: We hypothesize that alternate regulation of cyclooxygenase-2 (COX-2) may predispose patients to aspirin-induced exacerbations.Therefore, we want to examine the dynamics of COX-2 up-regulation in whole blood monocytes in the presence and absence of aspirin. Aspirin 108-115 prostaglandin-endoperoxide synthase 2 Homo sapiens 184-189 19295242-1 2009 BACKGROUND: We hypothesize that alternate regulation of cyclooxygenase-2 (COX-2) may predispose patients to aspirin-induced exacerbations.Therefore, we want to examine the dynamics of COX-2 up-regulation in whole blood monocytes in the presence and absence of aspirin. Aspirin 260-267 prostaglandin-endoperoxide synthase 2 Homo sapiens 56-72 19295242-1 2009 BACKGROUND: We hypothesize that alternate regulation of cyclooxygenase-2 (COX-2) may predispose patients to aspirin-induced exacerbations.Therefore, we want to examine the dynamics of COX-2 up-regulation in whole blood monocytes in the presence and absence of aspirin. Aspirin 260-267 prostaglandin-endoperoxide synthase 2 Homo sapiens 74-79 19295242-4 2009 RESULTS: We found significantly higher COX-2 expression levels after stimulation with LPS and aspirin (mean 78.8, range 44.9-92.3; p = 0.0002) in comparison to LPS alone (mean 65.9%, range 33.6-82.6) in AI patients. Aspirin 94-101 prostaglandin-endoperoxide synthase 2 Homo sapiens 39-44 18702823-1 2008 BACKGROUND: Epidemiologic and laboratory investigations suggest that aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) have chemopreventive effects against colon cancer perhaps due at least in part to their activity against cyclooxygenase-2 (COX-2), the rate-limiting enzyme of the prostaglandin cascade. Aspirin 69-76 prostaglandin-endoperoxide synthase 2 Homo sapiens 238-254 18702823-1 2008 BACKGROUND: Epidemiologic and laboratory investigations suggest that aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) have chemopreventive effects against colon cancer perhaps due at least in part to their activity against cyclooxygenase-2 (COX-2), the rate-limiting enzyme of the prostaglandin cascade. Aspirin 69-76 prostaglandin-endoperoxide synthase 2 Homo sapiens 256-261 18636671-0 2008 Mechanisms underlying aspirin-mediated growth inhibition and apoptosis induction of cyclooxygenase-2 negative colon cancer cell line SW480. Aspirin 22-29 prostaglandin-endoperoxide synthase 2 Homo sapiens 84-100 18483385-5 2008 RESULTS: Aspirin sensitized human breast cancer cells, but not untransformed human mammary epithelial cells, to TRAIL-induced caspase activation and apoptosis by a cyclooxygenase-2-independent mechanism. Aspirin 9-16 prostaglandin-endoperoxide synthase 2 Homo sapiens 164-180 17892525-7 2007 CONCLUSION: The increase in gastrointestinal hospitalization attributable to aspirin differed with the non-steroidal anti-inflammatory drug used, and seemed higher with cyclo-oxygenase-2 inhibitors than with non-selective non-steroidal anti-inflammatory drugs. Aspirin 77-84 prostaglandin-endoperoxide synthase 2 Homo sapiens 169-186 18058818-1 2008 Our previous study showed that aspirin induced apoptosis of esophageal cancer cells in vitro by inhibiting the pathway of NF-kappaB downstream regulation of cyclooxygenase-2. Aspirin 31-38 prostaglandin-endoperoxide synthase 2 Homo sapiens 157-173 17495879-7 2008 However, aspirin utilization appeared to modify the relationship between the PTGS2 G-765C polymorphism and CHD risk (interaction P=0.072). Aspirin 9-16 prostaglandin-endoperoxide synthase 2 Homo sapiens 77-82 18197933-6 2008 Both aspirin (5-20 mmol/L) and Nimesulide (0.1-0.8 mmol/L) inhibited EC-9706 cell line proliferation and suppressed its COX-2 mRNA expression dose-dependently. Aspirin 5-12 prostaglandin-endoperoxide synthase 2 Homo sapiens 120-125 18197933-7 2008 However, only aspirin (5-20 mmol/L) could inhibit proliferation in the EC-109 cell line and suppress COX-2 mRNA expression. Aspirin 14-21 prostaglandin-endoperoxide synthase 2 Homo sapiens 101-106 18167181-0 2007 Aspirin inhibits the proliferation of tobacco-related esophageal squamous carcinomas cell lines through cyclooxygenase 2 pathway. Aspirin 0-7 prostaglandin-endoperoxide synthase 2 Homo sapiens 104-120 18167181-4 2007 Whether aspirin can inhibit the proliferation of the ESCC cell lines pretreated with EE, and regulate the mRNA expression levels of COX-2 are also examined. Aspirin 8-15 prostaglandin-endoperoxide synthase 2 Homo sapiens 132-137 18167181-14 2007 However, the cell growth inhibition of aspirin was correlated with the down-regulation of COX-2 gene. Aspirin 39-46 prostaglandin-endoperoxide synthase 2 Homo sapiens 90-95 18209566-5 2008 The results showed that aspirin significantly suppressed COX-2 and ICAM-1 expression induced by ox-LDL and also inhibited IkappaB phosphorylation in human umbilical vein endothelial cells (HUVECs). Aspirin 24-31 prostaglandin-endoperoxide synthase 2 Homo sapiens 57-62 17663920-2 2007 OBJECTIVE: Our aim was to determine tolerance of Celecoxib, a selective inhibitor of cyclooxygenase-2 (Cox-2), by oral challenge test in patients who showed skin reactions (diffuse erythema or urticaria/angioedema) after taking ASA and/or NSAIDs. Aspirin 228-231 prostaglandin-endoperoxide synthase 2 Homo sapiens 103-108 17640058-3 2007 Prostaglandin H synthase 1 (PTGS1) and PTGS2 are key enzymes in prostaglandin synthesis and are inhibited by aspirin, whilst interleukin-10 (IL-10) is an important antiinflammatory cytokine. Aspirin 109-116 prostaglandin-endoperoxide synthase 2 Homo sapiens 39-44 17611980-0 2007 The effect of low-dose aspirin on the decreased risk of development of dyspepsia and gastrointestinal ulcers associated to cyclooxygenase-2 selective inhibitors. Aspirin 23-30 prostaglandin-endoperoxide synthase 2 Homo sapiens 123-139 17611980-1 2007 OBJECTIVE: To evaluate the risk of gastrointestinal (GI) symptoms and ulcers associated to the use of low-dose aspirin (ASA) among patients with rheumatoid arthritis (RA) and osteoarthritis (OA) treated with cyclooxygenase-2 (COX-2) drugs, to clarify the controversy in the literature. Aspirin 111-118 prostaglandin-endoperoxide synthase 2 Homo sapiens 208-224 17611980-1 2007 OBJECTIVE: To evaluate the risk of gastrointestinal (GI) symptoms and ulcers associated to the use of low-dose aspirin (ASA) among patients with rheumatoid arthritis (RA) and osteoarthritis (OA) treated with cyclooxygenase-2 (COX-2) drugs, to clarify the controversy in the literature. Aspirin 111-118 prostaglandin-endoperoxide synthase 2 Homo sapiens 226-231 17611980-1 2007 OBJECTIVE: To evaluate the risk of gastrointestinal (GI) symptoms and ulcers associated to the use of low-dose aspirin (ASA) among patients with rheumatoid arthritis (RA) and osteoarthritis (OA) treated with cyclooxygenase-2 (COX-2) drugs, to clarify the controversy in the literature. Aspirin 120-123 prostaglandin-endoperoxide synthase 2 Homo sapiens 208-224 17611980-1 2007 OBJECTIVE: To evaluate the risk of gastrointestinal (GI) symptoms and ulcers associated to the use of low-dose aspirin (ASA) among patients with rheumatoid arthritis (RA) and osteoarthritis (OA) treated with cyclooxygenase-2 (COX-2) drugs, to clarify the controversy in the literature. Aspirin 120-123 prostaglandin-endoperoxide synthase 2 Homo sapiens 226-231 17978563-0 2007 Copper-aspirin complex inhibits cyclooxygenase-2 more selectively than aspirin. Aspirin 7-14 prostaglandin-endoperoxide synthase 2 Homo sapiens 32-48 17589567-11 2007 Intake of ibuprofen or aspirin also produced significant risk reductions (OR=0.40, 95% CI=0.23-0.73 and OR=0.53, 95% CI=0.34-0.82, respectively), whereas acetaminophen, an analgesic with negligible COX-2 activity, had no effect on the risk (OR=1.36, 95% CI=0.53-3.37). Aspirin 23-30 prostaglandin-endoperoxide synthase 2 Homo sapiens 198-203 17522398-0 2007 Aspirin and the risk of colorectal cancer in relation to the expression of COX-2. Aspirin 0-7 prostaglandin-endoperoxide synthase 2 Homo sapiens 75-80 17522398-2 2007 METHODS: We estimated cyclooxygenase-2 (COX-2) expression by immunohistochemical assay of sections from paraffin-embedded colorectal-cancer specimens from two large cohorts of participants who provided data on aspirin use from a questionnaire every 2 years. Aspirin 210-217 prostaglandin-endoperoxide synthase 2 Homo sapiens 40-45 17522398-3 2007 We applied Cox regression to a competing-risks analysis to compare the effects of aspirin use on the relative risk of colorectal cancer in relation to the expression of COX-2 in the tumor. Aspirin 82-89 prostaglandin-endoperoxide synthase 2 Homo sapiens 169-174 17522398-6 2007 The effect of aspirin use differed significantly in relation to COX-2 expression (P for heterogeneity=0.02). Aspirin 14-21 prostaglandin-endoperoxide synthase 2 Homo sapiens 64-69 17522398-7 2007 Regular aspirin use conferred a significant reduction in the risk of colorectal cancers that overexpressed COX-2 (multivariate relative risk, 0.64; 95% confidence interval [CI], 0.52 to 0.78), whereas regular aspirin use had no influence on tumors with weak or absent expression of COX-2 (multivariate relative risk, 0.96; 95% CI, 0.73 to 1.26). Aspirin 8-15 prostaglandin-endoperoxide synthase 2 Homo sapiens 107-112 17522398-8 2007 The age-standardized incidence rate for cancers that overexpressed COX-2 was 37 per 100,000 person-years among regular aspirin users, as compared with 56 per 100,000 person-years among those who did not use aspirin regularly; in contrast, the rate for cancers with weak or absent COX-2 expression was 27 per 100,000 person-years among regular aspirin users, as compared with 28 per 100,000 person-years among nonregular aspirin users. Aspirin 119-126 prostaglandin-endoperoxide synthase 2 Homo sapiens 67-72 17522398-9 2007 CONCLUSIONS: Regular use of aspirin appears to reduce the risk of colorectal cancers that overexpress COX-2 but not the risk of colorectal cancers with weak or absent expression of COX-2. Aspirin 28-35 prostaglandin-endoperoxide synthase 2 Homo sapiens 102-107 17242290-0 2007 Letter by Kronish et al regarding article, "Residual arachidonic acid-induced platelet activation via an adenosine diphosphate-dependent but cyclooxygenase-1- and cyclooxygenase-2-independent pathway: a 700-patient study of aspirin resistance". Aspirin 224-231 prostaglandin-endoperoxide synthase 2 Homo sapiens 163-179 17329938-3 2007 The COX-2 pathway was activated by treating with serum-free medium for 12 h. The activated cells were incubated with NS398 (selective COX-2 inhibitor), SC560 (selective COX-1 inhibitor), acetyl salicylic acid (ASA) (nonselective COX inhibitor) at 37 degrees C for 15 min. Aspirin 187-208 prostaglandin-endoperoxide synthase 2 Homo sapiens 4-9 17329938-3 2007 The COX-2 pathway was activated by treating with serum-free medium for 12 h. The activated cells were incubated with NS398 (selective COX-2 inhibitor), SC560 (selective COX-1 inhibitor), acetyl salicylic acid (ASA) (nonselective COX inhibitor) at 37 degrees C for 15 min. Aspirin 210-213 prostaglandin-endoperoxide synthase 2 Homo sapiens 4-9 17488476-9 2007 Inhibition of Cox-2 by aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs) has been found to inhibit proliferation of colorectal cancer cells and in epidemiologic studies has been shown to reduce colon polyp formation in genetically predisposed populations and in the general population. Aspirin 23-30 prostaglandin-endoperoxide synthase 2 Homo sapiens 14-19 17301265-2 2007 Aspirin also inhibits the cyclooxygenase-2 enzyme and may share with n-3 fatty acids a potential mechanism to decrease the risk of colorectal cancer. Aspirin 0-7 prostaglandin-endoperoxide synthase 2 Homo sapiens 26-42 16792983-7 2006 COX-2 inhibitors, collectively called "coxibs" (celecoxib, rofecoxib, valdecoxib, lumiracoxib, etc), held a promise as anti-inflammatory drugs without the some of the side effects of aspirin or non steroidal antiinflammatory agents. Aspirin 183-190 prostaglandin-endoperoxide synthase 2 Homo sapiens 0-5 16951898-5 2006 Epi-lipoxins (epi-LXs), for instance, are produced from aspirin"s acetylation of inducible cyclooxygenase 2 (COX-2) and together with Resolvins represent an increasingly important family of immuno-regulatory and potentially cardio-protective lipid mediators. Aspirin 56-63 prostaglandin-endoperoxide synthase 2 Homo sapiens 91-107 16951898-5 2006 Epi-lipoxins (epi-LXs), for instance, are produced from aspirin"s acetylation of inducible cyclooxygenase 2 (COX-2) and together with Resolvins represent an increasingly important family of immuno-regulatory and potentially cardio-protective lipid mediators. Aspirin 56-63 prostaglandin-endoperoxide synthase 2 Homo sapiens 109-114 17037745-4 2006 RESULTS: RT-PCR showed that the expression COX-2 mRNA was strongly down-regulated in SKOV3 cells after treatment with Celecoxib or Aspirin. Aspirin 131-138 prostaglandin-endoperoxide synthase 2 Homo sapiens 43-48 17037745-5 2006 FCM and Western blot analysis showed that the protein product of COX-2 was strongly decreased by Celecoxib or Aspirin. Aspirin 110-117 prostaglandin-endoperoxide synthase 2 Homo sapiens 65-70 16785341-9 2006 CONCLUSIONS: There is a residual arachidonic acid-induced platelet activation in aspirin-treated patients that (1) is caused by underdosing and/or noncompliance in only approximately 2% of patients and (2) in the remaining patients, occurs via a cyclooxygenase-1 and cyclooxygenase-2 independent pathway, in direct proportion to the degree of baseline platelet activation, and is mediated in part by adenosine diphosphate-induced platelet activation. Aspirin 81-88 prostaglandin-endoperoxide synthase 2 Homo sapiens 267-283 16613568-3 2006 Acetylation of cyclooxygenase-2 (COX-2) by aspirin can trigger 15-epi-LXA4 (ATL) biosynthesis. Aspirin 43-50 prostaglandin-endoperoxide synthase 2 Homo sapiens 15-31 16529823-0 2006 Ascorbic acid enhances the inhibitory effect of aspirin on neuronal cyclooxygenase-2-mediated prostaglandin E2 production. Aspirin 48-55 prostaglandin-endoperoxide synthase 2 Homo sapiens 68-84 16529823-9 2006 Further, these experiments suggest that a combination of aspirin with ascorbic acid constitutes a novel approach to render COX-2 more sensitive to inhibition by aspirin, allowing an anti-inflammatory therapy with lower doses of aspirin, thereby avoiding the side effects of the usually high dose aspirin treatment. Aspirin 57-64 prostaglandin-endoperoxide synthase 2 Homo sapiens 123-128 16529823-9 2006 Further, these experiments suggest that a combination of aspirin with ascorbic acid constitutes a novel approach to render COX-2 more sensitive to inhibition by aspirin, allowing an anti-inflammatory therapy with lower doses of aspirin, thereby avoiding the side effects of the usually high dose aspirin treatment. Aspirin 161-168 prostaglandin-endoperoxide synthase 2 Homo sapiens 123-128 16529823-9 2006 Further, these experiments suggest that a combination of aspirin with ascorbic acid constitutes a novel approach to render COX-2 more sensitive to inhibition by aspirin, allowing an anti-inflammatory therapy with lower doses of aspirin, thereby avoiding the side effects of the usually high dose aspirin treatment. Aspirin 161-168 prostaglandin-endoperoxide synthase 2 Homo sapiens 123-128 16529823-9 2006 Further, these experiments suggest that a combination of aspirin with ascorbic acid constitutes a novel approach to render COX-2 more sensitive to inhibition by aspirin, allowing an anti-inflammatory therapy with lower doses of aspirin, thereby avoiding the side effects of the usually high dose aspirin treatment. Aspirin 161-168 prostaglandin-endoperoxide synthase 2 Homo sapiens 123-128 16613568-3 2006 Acetylation of cyclooxygenase-2 (COX-2) by aspirin can trigger 15-epi-LXA4 (ATL) biosynthesis. Aspirin 43-50 prostaglandin-endoperoxide synthase 2 Homo sapiens 33-38 16336399-0 2005 Aspirin induces apoptosis in oesophageal cancer cells by inhibiting the pathway of NF-kappaB downstream regulation of cyclooxygenase-2. Aspirin 0-7 prostaglandin-endoperoxide synthase 2 Homo sapiens 118-134 16480405-7 2006 More than two-thirds were aware that aspirin co-therapy decreased the GI safety benefits of the cyclo-oxygenase 2 selective NSAIDs. Aspirin 37-44 prostaglandin-endoperoxide synthase 2 Homo sapiens 96-113 16480405-8 2006 However, 84% felt that aspirin with a cyclo-oxygenase 2 selective NSAID was safer than aspirin with a non-selective NSAID. Aspirin 23-30 prostaglandin-endoperoxide synthase 2 Homo sapiens 38-55 16630404-12 2006 Exposure to nonsteroidal anti-inflammatory drugs/cyclooxygenase-2 inhibitors was associated with a reduced likelihood of prostate cancer (odds ratio [OR], 0.71; 95% confidence interval [CI], 0.58-0.86) as was exposure to aspirin (OR, 0.84; 95% CI, 0.74-0.96). Aspirin 221-228 prostaglandin-endoperoxide synthase 2 Homo sapiens 49-65 16175430-0 2006 The renal effects of the addition of low-dose aspirin to COX-2 selective and nonselective antiinflammatory drugs. Aspirin 46-53 prostaglandin-endoperoxide synthase 2 Homo sapiens 57-62 16493264-4 2006 The anti-tumor effects of aspirin and other NSAIDs are thought to arise primarily from an inhibition of cyclooxygenase-2. Aspirin 26-33 prostaglandin-endoperoxide synthase 2 Homo sapiens 104-120 16371720-2 2005 Aspirin was recently found to have chemopreventive effects on colon cancer and polyps by inhibiting cyclooxygenase-2. Aspirin 0-7 prostaglandin-endoperoxide synthase 2 Homo sapiens 100-116 16136765-1 2005 BACKGROUND: The use of selective inhibitors of cyclooxygenase 2 (COX-2) has been shown to be safe in patients with aspirin-induced asthma. Aspirin 115-122 prostaglandin-endoperoxide synthase 2 Homo sapiens 47-63 16136765-1 2005 BACKGROUND: The use of selective inhibitors of cyclooxygenase 2 (COX-2) has been shown to be safe in patients with aspirin-induced asthma. Aspirin 115-122 prostaglandin-endoperoxide synthase 2 Homo sapiens 65-70 15811906-1 2005 OBJECTIVE: To report the probable association of angioedema with aspirin therapy and the selective cyclooxygenase-2 (COX-2) inhibitor rofecoxib. Aspirin 65-72 prostaglandin-endoperoxide synthase 2 Homo sapiens 99-115 16101563-9 2005 COX-2 inhibitors, collectively called coxibs (celecoxib, rofecoxib, valdecoxib, lumiracoxib, etc), held a promise of improved treatment of arthritis without the gastrointestinal side effects associated with aspirin and other nonsteroidal anti-inflammatory drugs. Aspirin 207-214 prostaglandin-endoperoxide synthase 2 Homo sapiens 0-5 15955733-6 2005 Thus, epi-lipoxins, produced after aspirin acetylation of inducible cyclooxygenase-2, and glucocorticoid-regulated annexin 1 appear to be important endogenous mediators of their respective anti-inflammatory effects. Aspirin 35-42 prostaglandin-endoperoxide synthase 2 Homo sapiens 68-124 15811906-1 2005 OBJECTIVE: To report the probable association of angioedema with aspirin therapy and the selective cyclooxygenase-2 (COX-2) inhibitor rofecoxib. Aspirin 65-72 prostaglandin-endoperoxide synthase 2 Homo sapiens 117-122 15811906-8 2005 With skin testing and oral rechallenge with aspirin, but not rofecoxib, the allergist determined the cause of the reactions to be aspirin-induced angioedema and selective COX-2 inhibitor intolerance. Aspirin 44-51 prostaglandin-endoperoxide synthase 2 Homo sapiens 171-176 15811906-11 2005 There are reports of both tolerance and intolerance to selective COX-2 inhibitors in patients with documented allergy-like reactions to aspirin and NSAIDs. Aspirin 136-143 prostaglandin-endoperoxide synthase 2 Homo sapiens 65-70 15811906-12 2005 CONCLUSIONS: Patients with aspirin and NSAID intolerance may develop intolerance to COX-2 inhibitors, especially with repeated exposure. Aspirin 27-34 prostaglandin-endoperoxide synthase 2 Homo sapiens 84-89 15756426-0 2005 Aspirin, ibuprofen, and other non-steroidal anti-inflammatory drugs in cancer prevention: a critical review of non-selective COX-2 blockade (review). Aspirin 0-7 prostaglandin-endoperoxide synthase 2 Homo sapiens 125-130 15763541-0 2005 Dual effects of acetylsalicylic acid on mast cell degranulation, expression of cyclooxygenase-2 and release of pro-inflammatory cytokines. Aspirin 16-36 prostaglandin-endoperoxide synthase 2 Homo sapiens 79-95 15763541-4 2005 ASA blocked the expression of cyclooxygenase-2, the production of tumor necrosis factor-alpha and interleukin-6, and the release of granule mediators from mast cells in a concentration-dependent fashion. Aspirin 0-3 prostaglandin-endoperoxide synthase 2 Homo sapiens 30-46 15763541-8 2005 Interestingly, the expression of cyclooxygenase-2 was not inhibited at 1mM ASA, but was even enhanced significantly. Aspirin 75-78 prostaglandin-endoperoxide synthase 2 Homo sapiens 33-49 15741988-2 2005 The preventing effect of aspirin and nonsteroidal anti-inflammatory drugs is partly due to inhibition of the COX-2 enzyme. Aspirin 25-32 prostaglandin-endoperoxide synthase 2 Homo sapiens 109-114 15681294-5 2005 Recent advances in control of COX-2 transcription by aspirin and salicylate and by a cell cycle-dependent endogenous mechanism are described. Aspirin 53-60 prostaglandin-endoperoxide synthase 2 Homo sapiens 30-35 15811890-9 2005 NSAIDs with or without aspirin use are still associated with a significant risk of upper gastrointestinal bleeding in the era of cyclo-oxygenase 2 selective agents. Aspirin 23-30 prostaglandin-endoperoxide synthase 2 Homo sapiens 129-146 15345481-5 2005 Inhibition of COX-2 by acetyl salicylic acid (1 mM), NS-398 (5 microM), or celecoxib (3 microM) abolished the increase in cAMP and markedly reduced alpha(2C)-AR induction in response to serum stimulation. Aspirin 23-44 prostaglandin-endoperoxide synthase 2 Homo sapiens 14-19 15767339-10 2005 These data suggest that COX-2 expression or activity may be beneficially suppressed, and risk of colorectal polyps reduced, by aspirin or other NSAIDs in PTGS2 -765GG (wild type) individuals and by the -765 CC variant genotype in nonusers of NSAIDs. Aspirin 127-134 prostaglandin-endoperoxide synthase 2 Homo sapiens 24-29 15767339-10 2005 These data suggest that COX-2 expression or activity may be beneficially suppressed, and risk of colorectal polyps reduced, by aspirin or other NSAIDs in PTGS2 -765GG (wild type) individuals and by the -765 CC variant genotype in nonusers of NSAIDs. Aspirin 127-134 prostaglandin-endoperoxide synthase 2 Homo sapiens 154-159 17043507-7 2004 Aspirin increases the risk of NSAID-related gastrointestinal bleeding in patients taking COX-2 selective inhibitors, with odds ratios ranging from 5.8 to 7.7; however, it is unknown whether this risk is greater than the risk from aspirin alone. Aspirin 0-7 prostaglandin-endoperoxide synthase 2 Homo sapiens 89-94 16137190-13 2005 When patients with AIA need aspirin for specific situations they should receive aspirin desensitization therapy or treatment with selective cyclo-oxygenase 2 inhibitors. Aspirin 28-35 prostaglandin-endoperoxide synthase 2 Homo sapiens 140-157 15300570-7 2004 Addition of a cyclooxygenase-2 (COX-2) selective inhibitor to low-dose aspirin increased ulcer incidence, to a rate not significantly less than a nonselective nonsteroidal anti-inflammatory drug (NSAID) alone. Aspirin 71-78 prostaglandin-endoperoxide synthase 2 Homo sapiens 14-30 15300570-7 2004 Addition of a cyclooxygenase-2 (COX-2) selective inhibitor to low-dose aspirin increased ulcer incidence, to a rate not significantly less than a nonselective nonsteroidal anti-inflammatory drug (NSAID) alone. Aspirin 71-78 prostaglandin-endoperoxide synthase 2 Homo sapiens 32-37 15546508-6 2004 COX-2 protein expression and PGE(2) production were upregulated by ASA and indomethacin in all three cell lines. Aspirin 67-70 prostaglandin-endoperoxide synthase 2 Homo sapiens 0-5 17043507-8 2004 The risks from both traditional NSAIDs and COX-2 inhibitors are increased in the elderly, patients on anticoagulation, and patients with prior gastrointestinal events.Gastroprotective agents have been found to significantly reduce the risk for gastrointestinal injury in patients receiving NSAID therapy, especially those receiving concurrent low-dose cardioprotective doses of aspirin. Aspirin 378-385 prostaglandin-endoperoxide synthase 2 Homo sapiens 43-48 15242680-4 2004 Mechanistically, NO-aspirin, the best-studied NO-NSAID, has pleiotropic effects on cell signaling (it inhibits Wnt signaling, induces nitric oxide synthase and NF-kappaB activation and induces cyclooxygenase-2 expression), and this mechanistic redundancy might be central to its mode of action against cancer. Aspirin 20-27 prostaglandin-endoperoxide synthase 2 Homo sapiens 193-209 15213311-10 2004 Treatment of mesangial cells with LY294002 and cyclooxygenase-2 inhibitors [N-[2-(cyclohexyloxyl)-4-nitrophenyl]-methane sulfonamide (NS398) and aspirin] effectively inhibited the high glucose-induced mesangial cell proliferation. Aspirin 145-152 prostaglandin-endoperoxide synthase 2 Homo sapiens 47-63 14722849-5 2004 New results have confirmed the preventive effect of long-term aspirin use on adenoma recurrence, but the most cost-effective dosage is not clear; the mechanism of action is also uncertain, but seems to involve cyclooxygenase-2. Aspirin 62-69 prostaglandin-endoperoxide synthase 2 Homo sapiens 210-226 15167166-1 2004 BACKGROUND AND AIMS: Cyclooxygenase 2 (COX-2) is a target of aspirin and other non-steroidal anti-inflammatory drugs and is implicated in the pathogenesis of colorectal cancer. Aspirin 61-68 prostaglandin-endoperoxide synthase 2 Homo sapiens 21-37 15167166-1 2004 BACKGROUND AND AIMS: Cyclooxygenase 2 (COX-2) is a target of aspirin and other non-steroidal anti-inflammatory drugs and is implicated in the pathogenesis of colorectal cancer. Aspirin 61-68 prostaglandin-endoperoxide synthase 2 Homo sapiens 39-44 15056798-6 2004 Inhibition of mitogen-activated protein kinase kinase (MAPKK) and p38 MAPK using PD98059 (20 microM) and SB202190 (5 microM), respectively, attenuated the elevation of COX-2 protein induced by arsenite, whereas physiological concentrations of three COX-2 inhibitors (e.g., NS-398, piroxicam, and aspirin) reduced arsenite-stimulated DNA synthesis. Aspirin 296-303 prostaglandin-endoperoxide synthase 2 Homo sapiens 168-173 15144225-11 2004 COX-2 inhibitors NS398 and aspirin are capable of inhibiting the benzo[a]pyrene-induced osteoblast proliferation. Aspirin 27-34 prostaglandin-endoperoxide synthase 2 Homo sapiens 0-5 15120641-6 2004 Aspirin and rofecoxib (non-selective and selective COX-2 inhibitor, respectively) each abolished fibronectin-associated induction of MMP-2 and induced dose-dependent reductions in cellular invasiveness. Aspirin 0-7 prostaglandin-endoperoxide synthase 2 Homo sapiens 51-56 15043523-10 2004 CONCLUSIONS: In patients with increased susceptibility to gastrointestinal adverse events, a lower risk of upper gastrointestinal bleeding was observed in users of cyclo-oxygenase-2 inhibitors compared with users of other non-aspirin, non-steroidal anti-inflammatory drugs. Aspirin 226-233 prostaglandin-endoperoxide synthase 2 Homo sapiens 164-181 14519044-0 2003 Safety of COX-2 inhibitors in asthma patients with aspirin hypersensitivity. Aspirin 51-58 prostaglandin-endoperoxide synthase 2 Homo sapiens 10-15 14633677-0 2003 Growth inhibition of human colon cancer cells by nitric oxide (NO)-donating aspirin is associated with cyclooxygenase-2 induction and beta-catenin/T-cell factor signaling, nuclear factor-kappaB, and NO synthase 2 inhibition: implications for chemoprevention. Aspirin 76-83 prostaglandin-endoperoxide synthase 2 Homo sapiens 103-119 14519044-1 2003 OBJECTIVE: To review the safety of cyclooxygenase-2 (COX-2) inhibitors in asthma patients with aspirin hypersensitivity. Aspirin 95-102 prostaglandin-endoperoxide synthase 2 Homo sapiens 35-51 14519044-1 2003 OBJECTIVE: To review the safety of cyclooxygenase-2 (COX-2) inhibitors in asthma patients with aspirin hypersensitivity. Aspirin 95-102 prostaglandin-endoperoxide synthase 2 Homo sapiens 53-58 14519044-6 2003 DATA SYNTHESIS: The literature provides information regarding the safety of COX-2 inhibitors in asthma patients with aspirin-exacerbated respiratory disease (AERD). Aspirin 117-124 prostaglandin-endoperoxide synthase 2 Homo sapiens 76-81 12890715-0 2003 Evidence that 5-lipoxygenase and acetylated cyclooxygenase 2-derived eicosanoids regulate leukocyte-endothelial adherence in response to aspirin. Aspirin 137-144 prostaglandin-endoperoxide synthase 2 Homo sapiens 44-60 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 prostaglandin-endoperoxide synthase 2 Homo sapiens 129-145 14521608-9 2003 We found that colon cancer medium-induced COX-2 protein expression in EC and aspirin or sodium salicylate suppressed the cancer-induced COX-2 protein levels at concentrations correlated with those that suppressed endothelial tube formation. Aspirin 77-84 prostaglandin-endoperoxide synthase 2 Homo sapiens 136-141 14521608-10 2003 Furthermore, aspirin and sodium salicylate inhibited COX-2 expression stimulated by VEGF. Aspirin 13-20 prostaglandin-endoperoxide synthase 2 Homo sapiens 53-58 14521608-11 2003 These findings indicate that aspirin and other salicylate drugs at pharmacological concentrations inhibit colon cancer-induced angiogenesis which is correlated with COX-2 suppression. Aspirin 29-36 prostaglandin-endoperoxide synthase 2 Homo sapiens 165-170 12960371-0 2003 Interaction of a selective cyclooxygenase-2 inhibitor with aspirin and NO-releasing aspirin in the human gastric mucosa. Aspirin 59-66 prostaglandin-endoperoxide synthase 2 Homo sapiens 27-43 12960371-0 2003 Interaction of a selective cyclooxygenase-2 inhibitor with aspirin and NO-releasing aspirin in the human gastric mucosa. Aspirin 84-91 prostaglandin-endoperoxide synthase 2 Homo sapiens 27-43 12832097-2 2003 However, the mechanism by which ASA exhibits antiproliferative and proapoptotic effects in cyclooxygenase 2 (COX-2)-negative cells remains to be further elucidated. Aspirin 32-35 prostaglandin-endoperoxide synthase 2 Homo sapiens 91-107 12832097-2 2003 However, the mechanism by which ASA exhibits antiproliferative and proapoptotic effects in cyclooxygenase 2 (COX-2)-negative cells remains to be further elucidated. Aspirin 32-35 prostaglandin-endoperoxide synthase 2 Homo sapiens 109-114 12827217-4 2003 In addition, this compound inhibited cyclooxygenase-2 (COX-2) activity, which was also observed in aspirin-treated human monocytes. Aspirin 99-106 prostaglandin-endoperoxide synthase 2 Homo sapiens 37-53 12827217-4 2003 In addition, this compound inhibited cyclooxygenase-2 (COX-2) activity, which was also observed in aspirin-treated human monocytes. Aspirin 99-106 prostaglandin-endoperoxide synthase 2 Homo sapiens 55-60 12796206-0 2003 Cyclooxygenase-2 inhibitors in aspirin-sensitive asthma. Aspirin 31-38 prostaglandin-endoperoxide synthase 2 Homo sapiens 0-16 12743579-0 2003 Biochemical and clinical evidence that aspirin-intolerant asthmatic subjects tolerate the cyclooxygenase 2-selective analgetic drug celecoxib. Aspirin 39-46 prostaglandin-endoperoxide synthase 2 Homo sapiens 90-106 12870263-2 2003 The biological effects induced by aspirin and indomethacin on T98G cells, in which the expression of cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) were confirmed by RT-PCR and immunostaining, were investigated by studying cell proliferation and apoptosis assays. Aspirin 34-41 prostaglandin-endoperoxide synthase 2 Homo sapiens 130-146 12894587-4 2003 Inhibitors of the NF kappa B signaling pathway, which is activated by LMP-1, including I kappa B super-repressor and aspirin reduce or cancel induction of MMP-9, COX-2 and invasiveness of LMP-1-expressing cells. Aspirin 117-124 prostaglandin-endoperoxide synthase 2 Homo sapiens 162-167 12684334-0 2003 Cyclooxygenase-2 inhibitors in aspirin-induced asthma. Aspirin 31-38 prostaglandin-endoperoxide synthase 2 Homo sapiens 0-16 12622742-1 2003 BACKGROUND: We examined whether a decreased activity of nuclear factor(NF)-kappaB), a transcriptional regulator of cyclooxygenase-2 (COX-2), could account for down-regulation of COX-2 in nasal polyps of aspirin-sensitive asthmatics. Aspirin 203-210 prostaglandin-endoperoxide synthase 2 Homo sapiens 133-138 12668895-9 2003 The new highly selective cyclooxygenase 2 inhibitors are well tolerated in AERD asthmatics who have not been desensitized to aspirin. Aspirin 125-132 prostaglandin-endoperoxide synthase 2 Homo sapiens 25-41 12671901-3 2003 Aspirin acetylation of cyclooxygenase 2 also promotes the generation of a series of 15-epimers of LXA(4), known as aspirin-triggered lipoxins (ATL), that may account for some of the bioactivity profile of aspirin and possibly of nonsteroidal anti-inflammatory drugs. Aspirin 0-7 prostaglandin-endoperoxide synthase 2 Homo sapiens 23-39 12671901-3 2003 Aspirin acetylation of cyclooxygenase 2 also promotes the generation of a series of 15-epimers of LXA(4), known as aspirin-triggered lipoxins (ATL), that may account for some of the bioactivity profile of aspirin and possibly of nonsteroidal anti-inflammatory drugs. Aspirin 115-122 prostaglandin-endoperoxide synthase 2 Homo sapiens 23-39 12671901-3 2003 Aspirin acetylation of cyclooxygenase 2 also promotes the generation of a series of 15-epimers of LXA(4), known as aspirin-triggered lipoxins (ATL), that may account for some of the bioactivity profile of aspirin and possibly of nonsteroidal anti-inflammatory drugs. Aspirin 205-212 prostaglandin-endoperoxide synthase 2 Homo sapiens 23-39 12625225-0 2003 Impact of aspirin on the gastrointestinal-sparing effects of cyclooxygenase-2 inhibitors. Aspirin 10-17 prostaglandin-endoperoxide synthase 2 Homo sapiens 61-77 12622742-1 2003 BACKGROUND: We examined whether a decreased activity of nuclear factor(NF)-kappaB), a transcriptional regulator of cyclooxygenase-2 (COX-2), could account for down-regulation of COX-2 in nasal polyps of aspirin-sensitive asthmatics. Aspirin 203-210 prostaglandin-endoperoxide synthase 2 Homo sapiens 178-183 12622742-7 2003 CONCLUSION: This study shows that the low expression of COX-2 mRNA in nasal polyps from aspirin-sensitive patients is associated with a down-regulation of NF-kappaB activity. Aspirin 88-95 prostaglandin-endoperoxide synthase 2 Homo sapiens 56-61 14649387-5 2003 Aspirin is still required for patients with cardiovascular risk who are prescribed a COX-2-selective inhibitor. Aspirin 0-7 prostaglandin-endoperoxide synthase 2 Homo sapiens 85-90 12398900-6 2002 This finding indicates that specific PGHS-2 inhibitors are similar to ibuprofen in their ability to compete with aspirin, an irreversible time-dependent inhibitor of PGHS-1 often used for prevention of spontaneous thrombosis. Aspirin 113-120 prostaglandin-endoperoxide synthase 2 Homo sapiens 37-43 12428645-3 2002 Moreover, cyclooxygenase-2 is markedly downregulated in polyps from aspirin-sensitive patients with asthma. Aspirin 68-75 prostaglandin-endoperoxide synthase 2 Homo sapiens 10-26 12423325-0 2002 The effects of acetylsalicylic acid on proliferation, apoptosis, and invasion of cyclooxygenase-2 negative colon cancer cells. Aspirin 15-35 prostaglandin-endoperoxide synthase 2 Homo sapiens 81-97 12423325-3 2002 The aim of this study was to determine the effects of acetylsalicylic acid on proliferation, apoptosis, and invasion in human cyclooxygenase-2 (COX-2) negative colorectal cancer cell lines. Aspirin 54-74 prostaglandin-endoperoxide synthase 2 Homo sapiens 126-142 12423325-3 2002 The aim of this study was to determine the effects of acetylsalicylic acid on proliferation, apoptosis, and invasion in human cyclooxygenase-2 (COX-2) negative colorectal cancer cell lines. Aspirin 54-74 prostaglandin-endoperoxide synthase 2 Homo sapiens 144-149 12423325-14 2002 Down-regulation of Bcl2 expression might represent a potential mechanism by which ASA induces apoptosis in this COX-2 negative colon cancer cell line. Aspirin 82-85 prostaglandin-endoperoxide synthase 2 Homo sapiens 112-117 12466023-12 2002 This extends Aspirin"s mode of action from a covalent modification of COX-2 to the upstream regulation of COX-2 gene expression in neurons. Aspirin 13-20 prostaglandin-endoperoxide synthase 2 Homo sapiens 70-75 12466023-12 2002 This extends Aspirin"s mode of action from a covalent modification of COX-2 to the upstream regulation of COX-2 gene expression in neurons. Aspirin 13-20 prostaglandin-endoperoxide synthase 2 Homo sapiens 106-111 12398900-1 2002 Previous studies with both intact cells and ram seminal vesicles microsomes have shown that the specific PGHS-2 inhibitors NS-398 (N-[2-(cyclohexyloxy)-4-nitrophenyl]methanesulfonamide) and DuP-697 (5-bromo-2[4-fluorophenyl]-3-[4-methylsulfonylphenyl]-thiophene) attenuate the inhibition of PGHS-1 caused by aspirin and indomethacin. Aspirin 308-315 prostaglandin-endoperoxide synthase 2 Homo sapiens 105-111 12398900-7 2002 Importantly, the concentrations at which PGHS-2 inhibitors attenuate the inhibition induced by aspirin and indomethacin are well below those required to cause inhibition of PGHS-1. Aspirin 95-102 prostaglandin-endoperoxide synthase 2 Homo sapiens 41-47 17608990-5 2002 COX-2 inhibitors may be safe alternatives to traditional NSAIDs for patients with aspirin-sensitive asthma. Aspirin 82-89 prostaglandin-endoperoxide synthase 2 Homo sapiens 0-5 12167656-3 2002 In contrast, aspirin-treated PGHS-2 (ASA-PGHS-2) no longer forms prostaglandins but retains oxygenase activity forming 11(R)- and 15(R)-hydroperoxyeicosatetraenoic acid and also retains the EPR line-shape of the native peroxide-induced 29-30-G wide singlet radical. Aspirin 13-20 prostaglandin-endoperoxide synthase 2 Homo sapiens 29-35 12167656-3 2002 In contrast, aspirin-treated PGHS-2 (ASA-PGHS-2) no longer forms prostaglandins but retains oxygenase activity forming 11(R)- and 15(R)-hydroperoxyeicosatetraenoic acid and also retains the EPR line-shape of the native peroxide-induced 29-30-G wide singlet radical. Aspirin 13-20 prostaglandin-endoperoxide synthase 2 Homo sapiens 41-47 12167656-3 2002 In contrast, aspirin-treated PGHS-2 (ASA-PGHS-2) no longer forms prostaglandins but retains oxygenase activity forming 11(R)- and 15(R)-hydroperoxyeicosatetraenoic acid and also retains the EPR line-shape of the native peroxide-induced 29-30-G wide singlet radical. Aspirin 37-40 prostaglandin-endoperoxide synthase 2 Homo sapiens 29-35 12167656-3 2002 In contrast, aspirin-treated PGHS-2 (ASA-PGHS-2) no longer forms prostaglandins but retains oxygenase activity forming 11(R)- and 15(R)-hydroperoxyeicosatetraenoic acid and also retains the EPR line-shape of the native peroxide-induced 29-30-G wide singlet radical. Aspirin 37-40 prostaglandin-endoperoxide synthase 2 Homo sapiens 41-47 12167656-4 2002 To evaluate the functional role of the wide singlet radical in ASA-PGHS-2, we have examined the ability of this radical to oxidize AA in single-turnover EPR studies. Aspirin 63-66 prostaglandin-endoperoxide synthase 2 Homo sapiens 67-73 12065343-0 2002 Safety of a cyclooxygenase-2 inhibitor in patients with aspirin-sensitive asthma. Aspirin 56-63 prostaglandin-endoperoxide synthase 2 Homo sapiens 12-28 11964666-10 2001 Preliminary observations indicate that new, highly specific cyclooxygenase-2 inhibitors may soon become a safe alternative for aspirin-intolerant patients with asthma. Aspirin 127-134 prostaglandin-endoperoxide synthase 2 Homo sapiens 60-76 11717412-0 2001 A high level of cyclooxygenase-2 inhibitor selectivity is associated with a reduced interference of platelet cyclooxygenase-1 inactivation by aspirin. Aspirin 142-149 prostaglandin-endoperoxide synthase 2 Homo sapiens 16-32 11764357-7 2001 Results of the current study suggest that pain induction in osteoid osteoma is related to cyclooxygenase-2, an enzyme that is blocked by acetylsalicylic acid and rofecoxib. Aspirin 137-157 prostaglandin-endoperoxide synthase 2 Homo sapiens 90-106 11827359-7 2001 Use of low-dose aspirin concurrently with use of a selective cyclo-oxygenase-2 inhibitor may provide some degree of protection against the potential cardiovascular toxicity of the latter but both laboratory and clinical studies suggest that the concomitant use of these two types of drugs results in gastrointestinal ulceration comparable to what is seen with conventional non-steroidal anti-inflammatory drugs. Aspirin 16-23 prostaglandin-endoperoxide synthase 2 Homo sapiens 61-78 11695247-6 2001 They have raised the possibility that use of low dose aspirin may compromise these benefits and appear to have shown differences between (at least some) COX-2 inhibitors and (at least some) NSAIDs with regard to myocardial infarction. Aspirin 54-61 prostaglandin-endoperoxide synthase 2 Homo sapiens 153-158 11316217-1 2001 OBJECTIVE: Increased expression of the inducible cyclooxygenase 2 (COX-2) enzyme has been detected in esophageal and colonic adenocarcinoma, and intake of aspirin and non-steroidal anti-inflammatory drugs, known COX-2 inhibitors, have been associated with reduced tumor formation. Aspirin 155-162 prostaglandin-endoperoxide synthase 2 Homo sapiens 49-65 11316217-1 2001 OBJECTIVE: Increased expression of the inducible cyclooxygenase 2 (COX-2) enzyme has been detected in esophageal and colonic adenocarcinoma, and intake of aspirin and non-steroidal anti-inflammatory drugs, known COX-2 inhibitors, have been associated with reduced tumor formation. Aspirin 155-162 prostaglandin-endoperoxide synthase 2 Homo sapiens 67-72 11251623-1 2001 In a subset of patients with asthma, aspirin and several other non-steroidal anti-inflammatory drugs (NSAID) that inhibit simultaneously cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) precipitate dangerous asthmatic attacks. Aspirin 37-44 prostaglandin-endoperoxide synthase 2 Homo sapiens 166-182 11180079-7 2001 All four pancreatic cancer cell lines expressed COX-2 protein weakly or strongly, and the inhibitory effect of aspirin on cell growth was correlated with the expression of COX-2. Aspirin 111-118 prostaglandin-endoperoxide synthase 2 Homo sapiens 172-177 11235048-0 2001 Successful use of cyclooxygenase-2 inhibitor in a patient with aspirin-induced asthma. Aspirin 63-70 prostaglandin-endoperoxide synthase 2 Homo sapiens 18-34 11112909-0 2000 Selective cyclo-oxygenase 2 inhibitor in patients with aspirin-induced asthma. Aspirin 55-62 prostaglandin-endoperoxide synthase 2 Homo sapiens 10-27 11121721-0 2000 Synergistic inhibition of cyclooxygenase-2 expression by vitamin E and aspirin. Aspirin 71-78 prostaglandin-endoperoxide synthase 2 Homo sapiens 26-42 11121721-1 2000 The use of aspirin in rheumatoid arthritis is limited since inhibition of the pro-inflammatory enzyme cyclooxygenase-2 occurs only at higher aspirin doses that are often associated with side effects such as gastric toxicity. Aspirin 11-18 prostaglandin-endoperoxide synthase 2 Homo sapiens 102-118 11121721-1 2000 The use of aspirin in rheumatoid arthritis is limited since inhibition of the pro-inflammatory enzyme cyclooxygenase-2 occurs only at higher aspirin doses that are often associated with side effects such as gastric toxicity. Aspirin 141-148 prostaglandin-endoperoxide synthase 2 Homo sapiens 102-118 11121721-3 2000 1A), the present study explores possible synergistic effects of aspirin and vitamin E on the expression and activity of cyclooxygenase-2. Aspirin 64-71 prostaglandin-endoperoxide synthase 2 Homo sapiens 120-136 11121721-6 2000 Likewise, lipopolysaccharide-induced cyclooxygenase-2 protein and mRNA expression were virtually abolished by the combined treatment of aspirin and vitamin E, whereas the two agents alone were only modestly effective. Aspirin 136-143 prostaglandin-endoperoxide synthase 2 Homo sapiens 37-53 11121721-9 2000 Our results show that co-administration of vitamin E renders cyclooxygenase-2 more sensitive to inhibition by aspirin by as yet unknown mechanisms. Aspirin 110-117 prostaglandin-endoperoxide synthase 2 Homo sapiens 61-77 11142556-6 2000 Despite inhibiting of PGE2 generation, both nitric oxide-releasing derivatives and native aspirin and naproxen failed to affect expression of cyclooxygenase-1 mRNA but upregulated the cyclooxygenase-2 mRNA. Aspirin 90-97 prostaglandin-endoperoxide synthase 2 Homo sapiens 184-200 11192938-1 2000 Aspirin therapy inhibits prostaglandin biosynthesis; yet via acetylation of cyclooxygenase 2 (COX-2) it leads to bioactive lipoxins epimeric at carbon 15 (15-epi-LX, also termed aspirin-triggered lipoxin or ATL). Aspirin 178-185 prostaglandin-endoperoxide synthase 2 Homo sapiens 76-92 11192938-1 2000 Aspirin therapy inhibits prostaglandin biosynthesis; yet via acetylation of cyclooxygenase 2 (COX-2) it leads to bioactive lipoxins epimeric at carbon 15 (15-epi-LX, also termed aspirin-triggered lipoxin or ATL). Aspirin 178-185 prostaglandin-endoperoxide synthase 2 Homo sapiens 94-99 11192938-3 2000 Also, human endothelial cells, both HUVEC and microvascular, with upregulated COX-2 and treated with ASA converted C20:5 omega-3 to 18R-hydroxyeicosapentaenoic acid (HEPE) and 15R-HEPE. Aspirin 101-104 prostaglandin-endoperoxide synthase 2 Homo sapiens 78-83 11034610-1 2000 Aspirin therapy inhibits prostaglandin biosynthesis without directly acting on lipoxygenases, yet via acetylation of cyclooxygenase 2 (COX-2) it leads to bioactive lipoxins (LXs) epimeric at carbon 15 (15-epi-LX, also termed aspirin-triggered LX [ATL]). Aspirin 0-7 prostaglandin-endoperoxide synthase 2 Homo sapiens 135-140 11034610-1 2000 Aspirin therapy inhibits prostaglandin biosynthesis without directly acting on lipoxygenases, yet via acetylation of cyclooxygenase 2 (COX-2) it leads to bioactive lipoxins (LXs) epimeric at carbon 15 (15-epi-LX, also termed aspirin-triggered LX [ATL]). Aspirin 225-232 prostaglandin-endoperoxide synthase 2 Homo sapiens 117-133 11034610-1 2000 Aspirin therapy inhibits prostaglandin biosynthesis without directly acting on lipoxygenases, yet via acetylation of cyclooxygenase 2 (COX-2) it leads to bioactive lipoxins (LXs) epimeric at carbon 15 (15-epi-LX, also termed aspirin-triggered LX [ATL]). Aspirin 225-232 prostaglandin-endoperoxide synthase 2 Homo sapiens 135-140 11034610-3 2000 Human endothelial cells with upregulated COX-2 treated with ASA converted C20:5 omega-3 to 18R-hydroxyeicosapentaenoic acid (HEPE) and 15R-HEPE. Aspirin 60-63 prostaglandin-endoperoxide synthase 2 Homo sapiens 41-46 11078878-4 2000 This effect was more pronounced after inhibition of the cyclooxygenase-2 pathway by acetylsalicylic acid. Aspirin 84-104 prostaglandin-endoperoxide synthase 2 Homo sapiens 56-72 10404093-8 1999 We also observed a reduction of MSI phenotype after aspirin or sulindac treatment in a hMLH1-defective gastric cancer cell line SNU-1, which lacks COX-2 expression. Aspirin 52-59 prostaglandin-endoperoxide synthase 2 Homo sapiens 147-152 11040851-0 2000 The "aspirin" of the new millennium: cyclooxygenase-2 inhibitors. Aspirin 5-12 prostaglandin-endoperoxide synthase 2 Homo sapiens 37-53 10841038-4 2000 When these cells were pretreated with aspirin to inactivate their PGHS-1 and then activated by serum and phorbol ester (TPA) for 6 h, the cells expressed PGHS-2 activity alone. Aspirin 38-45 prostaglandin-endoperoxide synthase 2 Homo sapiens 154-160 10671506-4 2000 Aspirin treatment of cyclooxygenase-2 is known to acetylate an active site serine, block prostaglandin biosynthesis, and give 15R-hydroxyeicosatetraenoic acid (15R-HETE) as the only product. Aspirin 0-7 prostaglandin-endoperoxide synthase 2 Homo sapiens 21-37 10477832-0 1999 PGHS-2 inhibitors, NS-398 and DuP-697, attenuate the inhibition of PGHS-1 by aspirin and indomethacin without altering its activity. Aspirin 77-84 prostaglandin-endoperoxide synthase 2 Homo sapiens 0-6 10477832-8 1999 These results suggest that PGHS-2 inhibitors DuP-697 and NS-398 possibly interact with PGHS-1 at a site different from the enzyme"s catalytic site, thus causing attenuation of PGHS-1 inhibition by aspirin and indomethacin without altering PGHS-1 basal activity or the ibuprofen-induced inhibition. Aspirin 197-204 prostaglandin-endoperoxide synthase 2 Homo sapiens 27-33 10383505-0 1999 Specific inhibition of cyclooxygenase-2 with MK-0966 is associated with less gastroduodenal damage than either aspirin or ibuprofen. Aspirin 111-118 prostaglandin-endoperoxide synthase 2 Homo sapiens 23-39 10390414-0 1999 Cyclooxygenase-2 mRNA is downexpressed in nasal polyps from aspirin-sensitive asthmatics. Aspirin 60-67 prostaglandin-endoperoxide synthase 2 Homo sapiens 0-16 10093990-0 1999 Cyclooxygenase-2 in human platelets as a possible factor in aspirin resistance. Aspirin 60-67 prostaglandin-endoperoxide synthase 2 Homo sapiens 0-16 10220459-0 1999 Suppression of inducible cyclooxygenase 2 gene transcription by aspirin and sodium salicylate. Aspirin 64-71 prostaglandin-endoperoxide synthase 2 Homo sapiens 25-41 10101034-3 1999 However, only triflusal and aspirin inhibited purified COX-2 enzyme. Aspirin 28-35 prostaglandin-endoperoxide synthase 2 Homo sapiens 55-60 10101034-5 1999 This observation was further confirmed in a rat air pouch model in vivo, in which both aspirin and triflusal inhibited PGE2 production (ID50 = 18.9 and 11.4 mg/kg p.o., respectively) but only triflusal-treated animals showed a decrease in COX-2 expression. Aspirin 87-94 prostaglandin-endoperoxide synthase 2 Homo sapiens 239-244 9916892-7 1998 It is unabated, however, in the presence of substances inhibiting cyclooxygenase-1 and/or cyclooxygenase-2 (e.g., acetyl salicylic acid, SC 58125, L 745337), but is decreased by approx. Aspirin 114-135 prostaglandin-endoperoxide synthase 2 Homo sapiens 90-106 10073969-11 1999 Cox-2 and iNOS are coexpressed in native and transplant atherosclerosis, possibly allowing for interaction between the enzymes and suggesting an alternative mechanism for the benefits of aspirin via inhibition of Cox-2 activity. Aspirin 187-194 prostaglandin-endoperoxide synthase 2 Homo sapiens 0-5 10073969-11 1999 Cox-2 and iNOS are coexpressed in native and transplant atherosclerosis, possibly allowing for interaction between the enzymes and suggesting an alternative mechanism for the benefits of aspirin via inhibition of Cox-2 activity. Aspirin 187-194 prostaglandin-endoperoxide synthase 2 Homo sapiens 213-218 9809499-8 1998 Aspirin, but not acetaminophen, inhibits COX-2 activity. Aspirin 0-7 prostaglandin-endoperoxide synthase 2 Homo sapiens 41-46 9286937-8 1997 In contrast, aspirin could only inhibit monocyte PGHS-2 transiently at very high concentrations. Aspirin 13-20 prostaglandin-endoperoxide synthase 2 Homo sapiens 49-55 9288002-0 1997 In search of a better aspirin: suppression of intestinal polyposis by targeted inhibition of cyclooxygenase 2. Aspirin 22-29 prostaglandin-endoperoxide synthase 2 Homo sapiens 93-109 9686761-0 1998 Aspirin attenuates cytomegalovirus infectivity and gene expression mediated by cyclooxygenase-2 in coronary artery smooth muscle cells. Aspirin 0-7 prostaglandin-endoperoxide synthase 2 Homo sapiens 79-95 8898374-2 1996 We recently showed that ASA triggers the formation of a new series of potent bioactive eicosanoids, 15-epi-lipoxins (15-epi-LXs or ASA-triggered LX [ATL]), during interactions between prostaglandin endoperoxide synthase-2 (PGHS-2) in endothelial cells and 5-lipoxygenase (LO) in leukocytes. Aspirin 24-27 prostaglandin-endoperoxide synthase 2 Homo sapiens 184-221 9215309-9 1997 Aspirin attenuated the stimulatory effect of TPA on PGHS-2 promoter. Aspirin 0-7 prostaglandin-endoperoxide synthase 2 Homo sapiens 52-58 9215309-11 1997 The activity of PGHS-2 promoter is stimulated by either TPA or cAMP, and the stimulatory effect of TPA is attenuated by aspirin. Aspirin 120-127 prostaglandin-endoperoxide synthase 2 Homo sapiens 16-22 9048568-6 1997 Treatment of PGHS-2 with aspirin (acetyl salicylic acid, ASA) was previously shown to result in acetylation of a specific serine residue, cyclooxygenase inhibition, and increased lipoxygenase activity. Aspirin 25-32 prostaglandin-endoperoxide synthase 2 Homo sapiens 13-19 9048568-6 1997 Treatment of PGHS-2 with aspirin (acetyl salicylic acid, ASA) was previously shown to result in acetylation of a specific serine residue, cyclooxygenase inhibition, and increased lipoxygenase activity. Aspirin 34-55 prostaglandin-endoperoxide synthase 2 Homo sapiens 13-19 9048568-6 1997 Treatment of PGHS-2 with aspirin (acetyl salicylic acid, ASA) was previously shown to result in acetylation of a specific serine residue, cyclooxygenase inhibition, and increased lipoxygenase activity. Aspirin 57-60 prostaglandin-endoperoxide synthase 2 Homo sapiens 13-19 9048568-8 1997 We now have found the ASA-treated PGHS-2 radical to be indistinguishable from that in control PGHS-2. Aspirin 22-25 prostaglandin-endoperoxide synthase 2 Homo sapiens 34-40 9048568-9 1997 Addition of nimesulide to ASA-treated PGHS-2 inhibited the lipoxygenase and resulted in a narrow radical EPR like that seen in PGHS-2 treated with TNM or nimesulide alone. Aspirin 26-29 prostaglandin-endoperoxide synthase 2 Homo sapiens 38-44 9048568-9 1997 Addition of nimesulide to ASA-treated PGHS-2 inhibited the lipoxygenase and resulted in a narrow radical EPR like that seen in PGHS-2 treated with TNM or nimesulide alone. Aspirin 26-29 prostaglandin-endoperoxide synthase 2 Homo sapiens 127-133 9048568-11 1997 Both native and ASA-treated PGHS-2 produced only the R stereoisomer of 11- and 15-HETE, demonstrating that the lipoxygenase stereochemistry was not changed by ASA. Aspirin 16-19 prostaglandin-endoperoxide synthase 2 Homo sapiens 28-34 9048568-12 1997 Native and ASA-treated PGHS-2 had lipoxygenase K(m) values considerably higher than that of the control PGHS-2 cyclooxygenase. Aspirin 11-14 prostaglandin-endoperoxide synthase 2 Homo sapiens 23-29 9048568-12 1997 Native and ASA-treated PGHS-2 had lipoxygenase K(m) values considerably higher than that of the control PGHS-2 cyclooxygenase. Aspirin 11-14 prostaglandin-endoperoxide synthase 2 Homo sapiens 104-110 9048568-13 1997 Taken together, these results suggest that the same PGHS-2 tyrosyl radical serves as the oxidant for both cyclooxygenase and lipoxygenase catalysis and that acetylation of PGHS-2 by ASA favors arachidonate binding in an altered conformation which results in abstraction of the pro-R hydrogen from C13 and formation of 11(R)- and 15(R)-HETE. Aspirin 182-185 prostaglandin-endoperoxide synthase 2 Homo sapiens 52-58 9048568-13 1997 Taken together, these results suggest that the same PGHS-2 tyrosyl radical serves as the oxidant for both cyclooxygenase and lipoxygenase catalysis and that acetylation of PGHS-2 by ASA favors arachidonate binding in an altered conformation which results in abstraction of the pro-R hydrogen from C13 and formation of 11(R)- and 15(R)-HETE. Aspirin 182-185 prostaglandin-endoperoxide synthase 2 Homo sapiens 172-178 9016346-0 1997 Altered sensitivity of aspirin-acetylated prostaglandin G/H synthase-2 to inhibition by nonsteroidal anti-inflammatory drugs. Aspirin 23-30 prostaglandin-endoperoxide synthase 2 Homo sapiens 42-70 9016346-1 1997 Aspirin (ASA) acetylates Ser516 of prostaglandin G/H synthase-2 (PGHS-2) resulting in a modified enzyme that converts arachidonic acid to 15(R)-hydroxy-eicosatetraeroic acid [15(R)-HETE]. Aspirin 0-7 prostaglandin-endoperoxide synthase 2 Homo sapiens 35-63 9016346-1 1997 Aspirin (ASA) acetylates Ser516 of prostaglandin G/H synthase-2 (PGHS-2) resulting in a modified enzyme that converts arachidonic acid to 15(R)-hydroxy-eicosatetraeroic acid [15(R)-HETE]. Aspirin 0-7 prostaglandin-endoperoxide synthase 2 Homo sapiens 65-71 9016346-1 1997 Aspirin (ASA) acetylates Ser516 of prostaglandin G/H synthase-2 (PGHS-2) resulting in a modified enzyme that converts arachidonic acid to 15(R)-hydroxy-eicosatetraeroic acid [15(R)-HETE]. Aspirin 9-12 prostaglandin-endoperoxide synthase 2 Homo sapiens 35-63 9016346-1 1997 Aspirin (ASA) acetylates Ser516 of prostaglandin G/H synthase-2 (PGHS-2) resulting in a modified enzyme that converts arachidonic acid to 15(R)-hydroxy-eicosatetraeroic acid [15(R)-HETE]. Aspirin 9-12 prostaglandin-endoperoxide synthase 2 Homo sapiens 65-71 9016346-2 1997 ASA has pharmacological benefits that may not all be limited to inhibition of prostaglandin synthesis, and this study was initiated to further investigate the properties of ASA-acetylated PGHS-2 and of the mutation of Ser516 to methionine, which mimics ASA acetylation. Aspirin 173-176 prostaglandin-endoperoxide synthase 2 Homo sapiens 188-194 9016346-2 1997 ASA has pharmacological benefits that may not all be limited to inhibition of prostaglandin synthesis, and this study was initiated to further investigate the properties of ASA-acetylated PGHS-2 and of the mutation of Ser516 to methionine, which mimics ASA acetylation. Aspirin 173-176 prostaglandin-endoperoxide synthase 2 Homo sapiens 188-194 9016346-3 1997 Both the S516M mutant and ASA-acetylated form of PGHS-2 (ASA-PGHS-2) synthesize 15(R)-HETE and have apparent K(m) values for arachidonic acid within 10-fold of the apparent K(m) value for untreated PGHS-2. Aspirin 26-29 prostaglandin-endoperoxide synthase 2 Homo sapiens 49-55 9016346-3 1997 Both the S516M mutant and ASA-acetylated form of PGHS-2 (ASA-PGHS-2) synthesize 15(R)-HETE and have apparent K(m) values for arachidonic acid within 10-fold of the apparent K(m) value for untreated PGHS-2. Aspirin 26-29 prostaglandin-endoperoxide synthase 2 Homo sapiens 57-67 9016346-3 1997 Both the S516M mutant and ASA-acetylated form of PGHS-2 (ASA-PGHS-2) synthesize 15(R)-HETE and have apparent K(m) values for arachidonic acid within 10-fold of the apparent K(m) value for untreated PGHS-2. Aspirin 26-29 prostaglandin-endoperoxide synthase 2 Homo sapiens 61-67 9016346-8 1997 These results demonstrate that the sensitivity to inhibition by NSAIDs of the 15-HETE production by ASA-treated PGHS-2 is different than that of prostaglandin production by PGHS-2 and that Ser516 plays an important role in the interaction with fenamate inhibitors. Aspirin 100-103 prostaglandin-endoperoxide synthase 2 Homo sapiens 112-118 8898374-2 1996 We recently showed that ASA triggers the formation of a new series of potent bioactive eicosanoids, 15-epi-lipoxins (15-epi-LXs or ASA-triggered LX [ATL]), during interactions between prostaglandin endoperoxide synthase-2 (PGHS-2) in endothelial cells and 5-lipoxygenase (LO) in leukocytes. Aspirin 24-27 prostaglandin-endoperoxide synthase 2 Homo sapiens 223-229 8898374-2 1996 We recently showed that ASA triggers the formation of a new series of potent bioactive eicosanoids, 15-epi-lipoxins (15-epi-LXs or ASA-triggered LX [ATL]), during interactions between prostaglandin endoperoxide synthase-2 (PGHS-2) in endothelial cells and 5-lipoxygenase (LO) in leukocytes. Aspirin 131-134 prostaglandin-endoperoxide synthase 2 Homo sapiens 184-221 8898374-2 1996 We recently showed that ASA triggers the formation of a new series of potent bioactive eicosanoids, 15-epi-lipoxins (15-epi-LXs or ASA-triggered LX [ATL]), during interactions between prostaglandin endoperoxide synthase-2 (PGHS-2) in endothelial cells and 5-lipoxygenase (LO) in leukocytes. Aspirin 131-134 prostaglandin-endoperoxide synthase 2 Homo sapiens 223-229 8175750-0 1994 Acetylation of human prostaglandin endoperoxide synthase-2 (cyclooxygenase-2) by aspirin. Aspirin 81-88 prostaglandin-endoperoxide synthase 2 Homo sapiens 21-58 7568157-10 1995 These results demonstrate that ASA evokes a unique class of eicosanoids formed by acetylated PGHS-2 and 5-lipoxygenase interactions, which may contribute to the therapeutic impact of this drug. Aspirin 31-34 prostaglandin-endoperoxide synthase 2 Homo sapiens 93-99 7556619-0 1995 Comparison of recombinant cyclooxygenase-2 to native isoforms: aspirin labeling of the active site. Aspirin 63-70 prostaglandin-endoperoxide synthase 2 Homo sapiens 26-42 7610986-3 1995 The inducible form of PGHS, termed PGHS-2, has been purified and characterized with respect to substrate specificity, product formation, enzymatic activity, glycosylation, heme content, quaternary structure, and modification by aspirin. Aspirin 228-235 prostaglandin-endoperoxide synthase 2 Homo sapiens 35-41 8662657-3 1996 HUVEC treated with aspirin lost their capacity to generate PGs but recovery occurred after 3- or 6-h induction of Cox-2 with phorbol ester or IL-1alpha. Aspirin 19-26 prostaglandin-endoperoxide synthase 2 Homo sapiens 114-119 8662657-4 1996 Enzyme activity of the newly synthesized Cox-2 in aspirin-treated cells, evaluated after immunoprecipitation, was similar to untreated cells but after 18 h of cell stimulation only 50-60% recovery of Cox-1 was observed. Aspirin 50-57 prostaglandin-endoperoxide synthase 2 Homo sapiens 41-46 8662657-9 1996 However, in acetylsalicylic acid-treated cells, after 6-h stimulation with IL-1alpha, newly synthesized Cox-2 produced less TXB2 than 6-keto-PGF1alpha compared to untreated cells. Aspirin 12-32 prostaglandin-endoperoxide synthase 2 Homo sapiens 104-109 8175750-0 1994 Acetylation of human prostaglandin endoperoxide synthase-2 (cyclooxygenase-2) by aspirin. Aspirin 81-88 prostaglandin-endoperoxide synthase 2 Homo sapiens 60-76 8175750-2 1994 Aspirin treatment of hPGHS-2 produced an enzyme which retained oxygenase activity but formed exclusively 15-hydroxy-5,8,11,13-eicosatetraenoic acid (15-HETE) instead of PGH2. Aspirin 0-7 prostaglandin-endoperoxide synthase 2 Homo sapiens 21-28 8175750-4 1994 The Km values for arachidonate of native and aspirin-treated hPGHS-2 were about the same suggesting that arachidonate binds to both aspirin-treated and native hPGHS-2 in a similar manner. Aspirin 45-52 prostaglandin-endoperoxide synthase 2 Homo sapiens 61-68 8175750-4 1994 The Km values for arachidonate of native and aspirin-treated hPGHS-2 were about the same suggesting that arachidonate binds to both aspirin-treated and native hPGHS-2 in a similar manner. Aspirin 132-139 prostaglandin-endoperoxide synthase 2 Homo sapiens 61-68 8175750-8 1994 This indicates that Ser-516 is the site of aspirin acetylation of hPGHS-2; this residue is homologous to the "active site" serine of PGHS-1. Aspirin 43-50 prostaglandin-endoperoxide synthase 2 Homo sapiens 66-73 8175750-11 1994 An S516M mutant of hPGHS-2 was obtained which resembled aspirin-acetylated hPGHS-2 in that this mutant made 15R-HETE as its major product; however, unlike the aspirin-acetylated hPGHS-2, the Km value of the S516M mutant for arachidonate was 100 times that of native hPGHS-2. Aspirin 56-63 prostaglandin-endoperoxide synthase 2 Homo sapiens 19-26 8175750-11 1994 An S516M mutant of hPGHS-2 was obtained which resembled aspirin-acetylated hPGHS-2 in that this mutant made 15R-HETE as its major product; however, unlike the aspirin-acetylated hPGHS-2, the Km value of the S516M mutant for arachidonate was 100 times that of native hPGHS-2. Aspirin 56-63 prostaglandin-endoperoxide synthase 2 Homo sapiens 75-82 8175750-11 1994 An S516M mutant of hPGHS-2 was obtained which resembled aspirin-acetylated hPGHS-2 in that this mutant made 15R-HETE as its major product; however, unlike the aspirin-acetylated hPGHS-2, the Km value of the S516M mutant for arachidonate was 100 times that of native hPGHS-2. Aspirin 56-63 prostaglandin-endoperoxide synthase 2 Homo sapiens 75-82 8175750-11 1994 An S516M mutant of hPGHS-2 was obtained which resembled aspirin-acetylated hPGHS-2 in that this mutant made 15R-HETE as its major product; however, unlike the aspirin-acetylated hPGHS-2, the Km value of the S516M mutant for arachidonate was 100 times that of native hPGHS-2. Aspirin 56-63 prostaglandin-endoperoxide synthase 2 Homo sapiens 75-82 8175750-11 1994 An S516M mutant of hPGHS-2 was obtained which resembled aspirin-acetylated hPGHS-2 in that this mutant made 15R-HETE as its major product; however, unlike the aspirin-acetylated hPGHS-2, the Km value of the S516M mutant for arachidonate was 100 times that of native hPGHS-2. Aspirin 159-166 prostaglandin-endoperoxide synthase 2 Homo sapiens 19-26 8143845-0 1994 Mutation of serine-516 in human prostaglandin G/H synthase-2 to methionine or aspirin acetylation of this residue stimulates 15-R-HETE synthesis. Aspirin 78-85 prostaglandin-endoperoxide synthase 2 Homo sapiens 32-60 8143845-4 1994 While PG synthesis by both isoforms is inhibited by aspirin, 15-R-hydroxyeicosatetraenoic acid (15-R-HETE) synthesis by PGHS-2, but not PGHS-1, is stimulated by preincubation with aspirin. Aspirin 52-59 prostaglandin-endoperoxide synthase 2 Homo sapiens 120-126 8143845-4 1994 While PG synthesis by both isoforms is inhibited by aspirin, 15-R-hydroxyeicosatetraenoic acid (15-R-HETE) synthesis by PGHS-2, but not PGHS-1, is stimulated by preincubation with aspirin. Aspirin 180-187 prostaglandin-endoperoxide synthase 2 Homo sapiens 120-126 8143845-5 1994 We have mutated the putative aspirin acetylation site of hPGHS-2, and expressed the mutants in COS-7 cells using recombinant vaccinia virus. Aspirin 29-36 prostaglandin-endoperoxide synthase 2 Homo sapiens 57-64 8143845-6 1994 Enzyme activity and inhibitor sensitivity studies provide evidence that Ser516 is the aspirin acetylation site of human PGHS-2 and that substitution of a methionine residue at this position can mimic the effects of aspirin acetylation on enzyme activity. Aspirin 86-93 prostaglandin-endoperoxide synthase 2 Homo sapiens 120-126 8143845-6 1994 Enzyme activity and inhibitor sensitivity studies provide evidence that Ser516 is the aspirin acetylation site of human PGHS-2 and that substitution of a methionine residue at this position can mimic the effects of aspirin acetylation on enzyme activity. Aspirin 215-222 prostaglandin-endoperoxide synthase 2 Homo sapiens 120-126 35177224-14 2022 Cyclooxygenase-2 seems to be a downstream mediator between protease-activated receptor 1 and RhoA kinase because aspirin inhibits the nuclear translocation of nuclear factor-kappa B and inhibits neutrophil production of superoxide, thromboxane, and tumor necrosis factor alpha. Aspirin 113-120 prostaglandin-endoperoxide synthase 2 Homo sapiens 0-16 8114674-7 1994 Recombinant hPGHS-1 and hPGHS-2 both produced 15- and 11-hydroxyeicosatetraenoic acid (HETE) from arachidonic acid, with 15-HETE production by hPGHS-2 being stimulated 5-fold by preincubation with aspirin. Aspirin 197-204 prostaglandin-endoperoxide synthase 2 Homo sapiens 24-31 8114674-7 1994 Recombinant hPGHS-1 and hPGHS-2 both produced 15- and 11-hydroxyeicosatetraenoic acid (HETE) from arachidonic acid, with 15-HETE production by hPGHS-2 being stimulated 5-fold by preincubation with aspirin. Aspirin 197-204 prostaglandin-endoperoxide synthase 2 Homo sapiens 143-150 8114674-8 1994 Chiral phase high performance liquid chromatography analysis showed that aspirin-treated hPGHS-2 produced 15(R)-HETE, with no detectable 15(S)-HETE. Aspirin 73-80 prostaglandin-endoperoxide synthase 2 Homo sapiens 89-96 34700376-7 2021 In HCAE cells, overexpressed genes included EFNA1 and LIF, two genes commonly upregulated in colorectal cancer and associated with poor patient outcomes, and PTGS2 (COX2), a gene associated with the protective effect of aspirin in the colorectal cancer setting. Aspirin 220-227 prostaglandin-endoperoxide synthase 2 Homo sapiens 158-163 34168274-8 2021 The hub targets for aspirin in preventing preeclampsia were tumor protein p53 (TP53), C-X-C motif chemokine ligand 8 (CXCL8), mitogen-activated protein kinase 3 (MAPK3), mitogen-activated protein kinase 1 (MAPK1), mitogen-activated protein kinase 14 (MAPK14), epidermal growth factor receptor (EGFR), estrogen receptor (ESR1), and prostaglandin-endoperoxide synthase 2 (PTGS2). Aspirin 20-27 prostaglandin-endoperoxide synthase 2 Homo sapiens 331-368 34168274-8 2021 The hub targets for aspirin in preventing preeclampsia were tumor protein p53 (TP53), C-X-C motif chemokine ligand 8 (CXCL8), mitogen-activated protein kinase 3 (MAPK3), mitogen-activated protein kinase 1 (MAPK1), mitogen-activated protein kinase 14 (MAPK14), epidermal growth factor receptor (EGFR), estrogen receptor (ESR1), and prostaglandin-endoperoxide synthase 2 (PTGS2). Aspirin 20-27 prostaglandin-endoperoxide synthase 2 Homo sapiens 370-375 26335632-11 2015 Cyclooxygenase-2 gene expression decreased compared to controls during DHA stimulation after 72 h. Treatment with DHA and ASA revealed a decreased 15-lipoxygenase gene expression which was reduced after three days of DHA incubation. Aspirin 122-125 prostaglandin-endoperoxide synthase 2 Homo sapiens 0-16 34540977-8 2021 Aspirin has been reported to suppress the Wnt pathway by inducing beta-catenin phosphorylation through the activation of glycogen synthase kinase 3 beta via cyclooxygenase-2 pathway inhibition. Aspirin 0-7 prostaglandin-endoperoxide synthase 2 Homo sapiens 157-173 34127813-7 2021 The suppression of cell apoptosis by ASPN overexpression could be attenuated by LEF1 knockdown or 100 microM aspirin (PTGS2 inhibitor), and siASPN mediated apoptosis could be rescued by LEF1 ectopic expression or adding recombinant IL6. Aspirin 109-116 prostaglandin-endoperoxide synthase 2 Homo sapiens 118-123 35470674-0 2022 Acetylsalicylic Acid Is Associated With a Lower Prevalence of Ascending Aortic Aneurysm and a Decreased Aortic Expression of Cyclooxygenase 2. Aspirin 0-20 prostaglandin-endoperoxide synthase 2 Homo sapiens 125-141 35470674-9 2022 In dilated, but not nondilated tricuspid aortic valve aortic specimens, ASA was associated with significantly lower cyclooxygenase-2 levels (P=0.034). Aspirin 72-75 prostaglandin-endoperoxide synthase 2 Homo sapiens 116-132 35470674-10 2022 Conclusions Our findings are consistent with the hypothesis that ASA treatment may attenuate ascending aortic aneurysmal growth, possibly via cyclooxygenase-2 inhibition in the ascending aortic wall and subsequent anti-inflammatory actions. Aspirin 65-68 prostaglandin-endoperoxide synthase 2 Homo sapiens 142-158 31696583-3 2020 The synthesis of aspirin-triggered lipoxin (ATL) by cyclooxygenase-2 acetylation is an alternative mechanism of ASA, which could explain the effectiveness of ASA treatments. Aspirin 17-24 prostaglandin-endoperoxide synthase 2 Homo sapiens 52-68 33430037-10 2021 PTGS2/COX2 expression trended lower in aspirin users, but not with tumor response. Aspirin 39-46 prostaglandin-endoperoxide synthase 2 Homo sapiens 0-5 33360326-4 2021 The cyclooxygenase-2 enzyme inhibited by Aspirin and other NSAIDs, and which catalyses prostaglandin synthesis and mediates inflammation, is overexpressed in prostate cancer, therefore inhibition of cyclooxygenase-2 may have direct, and indirect, therapeutic effects. Aspirin 41-48 prostaglandin-endoperoxide synthase 2 Homo sapiens 4-20 33360326-4 2021 The cyclooxygenase-2 enzyme inhibited by Aspirin and other NSAIDs, and which catalyses prostaglandin synthesis and mediates inflammation, is overexpressed in prostate cancer, therefore inhibition of cyclooxygenase-2 may have direct, and indirect, therapeutic effects. Aspirin 41-48 prostaglandin-endoperoxide synthase 2 Homo sapiens 199-215 33038835-4 2020 A focus is also done on single lipoxygenation of mono-hydroxylated products first made by aspirin-treated cyclooxygenase-2. Aspirin 90-97 prostaglandin-endoperoxide synthase 2 Homo sapiens 106-122 32535107-0 2020 Characterization of cyclooxygenase-2 acetylation and prostanoid inhibition by aspirin in cellular systems. Aspirin 78-85 prostaglandin-endoperoxide synthase 2 Homo sapiens 20-36 32646396-13 2020 In addition, the survival benefit of postdiagnosis aspirin use appeared to be confined to patients with mutated PIK3CA tumors [HR = 0.78, 95%CI(0.50, 0.99)] and was positive for PTGS2 (COX-2) expression [HR = 0.75, 95%CI(0.43, 1.30)]. Aspirin 51-58 prostaglandin-endoperoxide synthase 2 Homo sapiens 178-183 32646396-14 2020 CONCLUSIONS: These findings provide further indications that postdiagnosis aspirin use improves overall survival and cancer-specific survival in colorectal cancer, especially for patients who are positive for PTGS2 (COX-2) expression and PIK3CA-mutated tumors. Aspirin 75-82 prostaglandin-endoperoxide synthase 2 Homo sapiens 209-214 32181121-5 2020 Molecular docking and nonbonding interactions have been performed against human cyclooxygenase-2 protein 5F1A to investigate the binding affinity and mode(s) of newly designed aspirin derivatives. Aspirin 176-183 prostaglandin-endoperoxide synthase 2 Homo sapiens 80-96 31696583-3 2020 The synthesis of aspirin-triggered lipoxin (ATL) by cyclooxygenase-2 acetylation is an alternative mechanism of ASA, which could explain the effectiveness of ASA treatments. Aspirin 112-115 prostaglandin-endoperoxide synthase 2 Homo sapiens 52-68 31696583-3 2020 The synthesis of aspirin-triggered lipoxin (ATL) by cyclooxygenase-2 acetylation is an alternative mechanism of ASA, which could explain the effectiveness of ASA treatments. Aspirin 158-161 prostaglandin-endoperoxide synthase 2 Homo sapiens 52-68 31356853-3 2019 The aim of this study was to demonstrate the synthesis of a new compound bearing salicylic acid residue namely 2-((3-(chloromethyl)benzoyl)oxy)benzoic acid, to analyze its potential as a ligand for human cyclooxygenase-2 (COX-2) receptor, to evaluate its toxicity level and its effectiveness for analgesic and antiplatelet agent compared with acetylsalicylic acid. Aspirin 343-363 prostaglandin-endoperoxide synthase 2 Homo sapiens 204-220 29781520-6 2018 A significant association with poor responsiveness to aspirin was observed for GP1BA rs2243093, PTGS1 rs1330344, PTGS2 rs689466 and TBXA2R rs1131882 polymorphisms in overall analyses. Aspirin 54-61 prostaglandin-endoperoxide synthase 2 Homo sapiens 113-118 31234130-5 2019 Further, a comparative molecular modeling analysis of TM-7 carried out with the crystal structure of aspirin acetylated human COX-2 suggested effectively binding and efficient accommodation inside the active site"s gorge. Aspirin 101-108 prostaglandin-endoperoxide synthase 2 Homo sapiens 126-131 31291992-1 2019 Acetylsalicylic acid has been linked to a lower risk for different cancer types, presumably through its inhibitory effect on cyclooxygenase 2. Aspirin 0-20 prostaglandin-endoperoxide synthase 2 Homo sapiens 125-141 29718107-8 2018 However, ASP administration impeded NF-kappaB signaling activation, downregulated COX-2 and inflammatory factor expression, and rescued trophoblast invasion. Aspirin 9-12 prostaglandin-endoperoxide synthase 2 Homo sapiens 82-87 30149368-3 2018 The cyclooxygenase-2 (COX-2) inhibitory and other direct and indirect pathways of aspirin are translated to inhibition proliferation and enhanced apoptosis of cancer cells. Aspirin 82-89 prostaglandin-endoperoxide synthase 2 Homo sapiens 22-27 30131302-6 2018 Mechanistic studies revealed that the reduction of cox2 by aspirin in A549 and H1299 was caused by disruption of the chromosomal architecture of the cox2 locus. Aspirin 59-66 prostaglandin-endoperoxide synthase 2 Homo sapiens 51-55 30131302-6 2018 Mechanistic studies revealed that the reduction of cox2 by aspirin in A549 and H1299 was caused by disruption of the chromosomal architecture of the cox2 locus. Aspirin 59-66 prostaglandin-endoperoxide synthase 2 Homo sapiens 149-153 29392539-9 2018 The effects of metformin and aspirin partly relied on cyclooxygenase-2 (COX-2) upregulation, without the production of lipoxins. Aspirin 29-36 prostaglandin-endoperoxide synthase 2 Homo sapiens 54-70 29392539-9 2018 The effects of metformin and aspirin partly relied on cyclooxygenase-2 (COX-2) upregulation, without the production of lipoxins. Aspirin 29-36 prostaglandin-endoperoxide synthase 2 Homo sapiens 72-77 30149368-3 2018 The cyclooxygenase-2 (COX-2) inhibitory and other direct and indirect pathways of aspirin are translated to inhibition proliferation and enhanced apoptosis of cancer cells. Aspirin 82-89 prostaglandin-endoperoxide synthase 2 Homo sapiens 4-20 29599304-1 2018 Aspirin has cyclooxygenase-2 (COX2)-mediated anti-inflammatory and anti-coagulant properties that may confer a positive effect in preventing and limiting the progression of prostate cancer. Aspirin 0-7 prostaglandin-endoperoxide synthase 2 Homo sapiens 12-28 29599304-1 2018 Aspirin has cyclooxygenase-2 (COX2)-mediated anti-inflammatory and anti-coagulant properties that may confer a positive effect in preventing and limiting the progression of prostate cancer. Aspirin 0-7 prostaglandin-endoperoxide synthase 2 Homo sapiens 30-34 29599304-2 2018 Prostate cancer has been shown to have poor treatment outcomes due to therapeutic resistance; therefore, COX2 inhibition caused by aspirin could represent an opportunity to augment current therapies. Aspirin 131-138 prostaglandin-endoperoxide synthase 2 Homo sapiens 105-109