PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 22371762-3 2010 Recently, we demonstrated that morphine administration in vitro resulted in decreased cellular concentrations of COMT-encoding mRNA levels, as compared to control values. Morphine 31-39 catechol-O-methyltransferase Homo sapiens 113-117 22371762-5 2010 In sum, these observations indicate a potential reciprocal linkage between end product inhibition of COMT gene expression by E and morphine. Morphine 131-139 catechol-O-methyltransferase Homo sapiens 101-105 17573783-0 2008 Endogenous morphine signaling via nitric oxide regulates the expression of CYP2D6 and COMT: autocrine/paracrine feedback inhibition. Morphine 11-19 catechol-O-methyltransferase Homo sapiens 86-90 19912274-7 2010 Given the striking similarities between the enzymatic steps in the morphine biosynthetic pathway and those driving the evolutionary adaptation of catecholamine chemical species to accommodate an expansion of interactive but distinct signaling systems, it is our overall contention that the evolutionary emergence of catecholamine systems required conservation and selective "retrofit" of specific enzyme activities, that is, COMT, drawn from cellular morphine expression. Morphine 67-75 catechol-O-methyltransferase Homo sapiens 425-429 18257092-0 2008 Genetic variation and response to morphine in cancer patients: catechol-O-methyltransferase and multidrug resistance-1 gene polymorphisms are associated with central side effects. Morphine 34-42 catechol-O-methyltransferase Homo sapiens 63-91 18257092-11 2008 CONCLUSIONS: COMT and MDR-1 genotypes were correlated with morphine-related central side effects. Morphine 59-67 catechol-O-methyltransferase Homo sapiens 13-17 20150871-2 2010 The genes/enzymes (CYP2D6, COMT and PNMT) that are involved in the biosynthesis of morphine have variations that affect their functionality. Morphine 83-91 catechol-O-methyltransferase Homo sapiens 27-31 19094200-4 2008 It is shown that a polymorphism in the COMT gene, Rs4680 (Val158Met), influence pain sensitivity in human experimental pain and the efficacy for morphine in cancer pain treatment. Morphine 145-153 catechol-O-methyltransferase Homo sapiens 39-43 19094200-5 2008 In this study we wanted to investigate if variability in other regions in the COMT gene also contributes to interindividual variability in morphine efficacy. Morphine 139-147 catechol-O-methyltransferase Homo sapiens 78-82 19094200-11 2008 CONCLUSION: This study suggests that genetic variability in the COMT gene influence the efficacy of morphine in cancer patients with pain, and that increased understanding of this variability is reached by expanding from analyses of single SNPs to haplotype construction and analyses. Morphine 100-108 catechol-O-methyltransferase Homo sapiens 64-68 17722074-3 2008 Emerging evidence suggests that the allelic variants in the genes involving the opioid (UGT2B7, OPRM1, and ABCB1 genes) and nonopioid system (COMT gene) can alter the efficacy of morphine. Morphine 179-187 catechol-O-methyltransferase Homo sapiens 142-146 17573783-2 2008 Leukocyte exposure to morphine down-regulated catechol-O-methyl transferase (COMT) and CYP2D6 by approximately 50% compared with control values. Morphine 22-30 catechol-O-methyltransferase Homo sapiens 46-75 17573783-2 2008 Leukocyte exposure to morphine down-regulated catechol-O-methyl transferase (COMT) and CYP2D6 by approximately 50% compared with control values. Morphine 22-30 catechol-O-methyltransferase Homo sapiens 77-81 17573783-4 2008 The verification of the microarray data was accomplished via real-time Taqman reverse transcriptase polymerase chain reaction (RT-PCR) focused on CYP2D6 and COMT expression in different blood samples treated with morphine. Morphine 213-221 catechol-O-methyltransferase Homo sapiens 157-161 17982691-5 2007 Given the striking similarities between the enzymatic steps in the morphine biosynthetic pathway and those driving the evolutionary adaptation of catecholamine chemical species to accommodate an expansion of interactive but distinct signaling systems, we surmise that the evolutionary emergence of catecholamine systems required conservation and selective "retrofit" of specific enzyme activities, i.e. catechol O-methyl transferase and phenylethanol-amine N-methyl transferase, drawn from cellular morphine expression. Morphine 67-75 catechol-O-methyltransferase Homo sapiens 403-432 18370847-6 2008 The COMT V158M variant has been associated with decreased morphine requirements for analgesia. Morphine 58-66 catechol-O-methyltransferase Homo sapiens 4-8 16215614-4 2005 Furthermore, variability in an enzyme-degrading catecholamines (COMT gene) may also alter the efficacy of morphine, which shows that genetic variability in non-opioid systems may indirectly influence the clinical opioid efficacy. Morphine 106-114 catechol-O-methyltransferase Homo sapiens 64-68 17156920-0 2007 Exploring joint effects of genes and the clinical efficacy of morphine for cancer pain: OPRM1 and COMT gene. Morphine 62-70 catechol-O-methyltransferase Homo sapiens 98-102 17156920-4 2007 We assessed joint effects of the OPRM1 and COMT genes in predicting morphine dose for cancer pain relief. Morphine 68-76 catechol-O-methyltransferase Homo sapiens 43-47 17156920-6 2007 Results showed significant variation in morphine dose requirement by genotype groups: carriers of COMT Val/Val and Val/Met genotype required 63% and 23%, respectively, higher morphine dose compared to carriers of Met/Met genotype (p=0.02). Morphine 40-48 catechol-O-methyltransferase Homo sapiens 98-102 17156920-6 2007 Results showed significant variation in morphine dose requirement by genotype groups: carriers of COMT Val/Val and Val/Met genotype required 63% and 23%, respectively, higher morphine dose compared to carriers of Met/Met genotype (p=0.02). Morphine 175-183 catechol-O-methyltransferase Homo sapiens 98-102 17156920-8 2007 When we explored for joint effects, we found that carriers of the OPRM1 AA and COMT Met/Met genotype required the lowest morphine dose to achieve pain relief (87 mg/24 h; 95%CI=57,116) and those with neither Met/Met nor AA genotype needed the highest morphine dose (147 mg/24 h; 95%CI=100,180). Morphine 121-129 catechol-O-methyltransferase Homo sapiens 79-83 15927391-4 2005 Based on this information we analyzed the influence from the COMT Val158Met polymorphism on the efficacy of morphine in a cohort of patients suffering from cancer pain. Morphine 108-116 catechol-O-methyltransferase Homo sapiens 61-65 16045647-4 2005 Furthermore, variability in an enzyme degrading catecholamines (COMT gene) alters the efficacy of morphine demonstrating that genetic variability in non-opioid systems may indirectly influence the clinical efficacy from morphine. Morphine 98-106 catechol-O-methyltransferase Homo sapiens 64-68 16045647-4 2005 Furthermore, variability in an enzyme degrading catecholamines (COMT gene) alters the efficacy of morphine demonstrating that genetic variability in non-opioid systems may indirectly influence the clinical efficacy from morphine. Morphine 220-228 catechol-O-methyltransferase Homo sapiens 64-68 15927391-0 2005 The Val158Met polymorphism of the human catechol-O-methyltransferase (COMT) gene may influence morphine requirements in cancer pain patients. Morphine 95-103 catechol-O-methyltransferase Homo sapiens 40-68 15927391-0 2005 The Val158Met polymorphism of the human catechol-O-methyltransferase (COMT) gene may influence morphine requirements in cancer pain patients. Morphine 95-103 catechol-O-methyltransferase Homo sapiens 70-74 15927391-8 2005 These results suggest that genetic variation in the COMT gene may contribute to variability in the efficacy of morphine in cancer pain treatment. Morphine 111-119 catechol-O-methyltransferase Homo sapiens 52-56 29870475-0 2018 Severe and persistent morphine-induced respiratory depression associated with ATP-Binding Cassette Subfamily B Member 1 and catechol-O-methyltransferase genetic defects: A case report. Morphine 22-30 catechol-O-methyltransferase Homo sapiens 124-152 34015137-8 2021 However, in Indian patients, 41% of morphine consumption variability could be explained by age (explaining <3%) and variants in OPRM1 rs1799971, CRP rs2794521, TLR4 rs4986790, IL2 rs2069762, COMT rs4818, TGFB1 rs1800469 and IL6R rs8192284 when not controlling for postoperative pain. Morphine 36-44 catechol-O-methyltransferase Homo sapiens 191-195 31967515-3 2020 Results: Patients in the fentanyl group with the COMT high-pain sensitivity haplotype required less postoperative morphine compared with the average-pain sensitivity haplotype (19.4 [16.5; 23.0] vs 34.6 [26.2; 41.4]; p = 0.00768), but not to the low-pain sensitivity group (30.1 [19.1; 37.7]; p = 0.13). Morphine 114-122 catechol-O-methyltransferase Homo sapiens 49-53 30709768-8 2019 More Externalizing behaviour was predicted by greater morphine exposure in children with the COMT rs4680 Met/Met genotype (p = 0006). Morphine 54-62 catechol-O-methyltransferase Homo sapiens 93-97 29259946-4 2017 Methods: This prospective association study investigated seven variations in the OPRM1, OPRK1 and COMT gene, which encode Mu and KAPPA opioid receptors, and Catechol-O-methyltransferase enzyme respectively, in a cohort of 129 Tunisian cancer pain patients under oral morphine treatment. Morphine 267-275 catechol-O-methyltransferase Homo sapiens 98-102 28928973-0 2017 Prospective replication study implicates the catechol-O-methyltransferase Val158Met polymorphism as a biomarker for the response to morphine in patients with cancer. Morphine 132-140 catechol-O-methyltransferase Homo sapiens 45-73 28985716-3 2017 We previously showed that the catechol-O-methyltransferase (COMT) genotype is related to the plasma level of morphine and the required dose of morphine in an exploratory prospective study. Morphine 109-117 catechol-O-methyltransferase Homo sapiens 30-58 28985716-3 2017 We previously showed that the catechol-O-methyltransferase (COMT) genotype is related to the plasma level of morphine and the required dose of morphine in an exploratory prospective study. Morphine 109-117 catechol-O-methyltransferase Homo sapiens 60-64 28985716-3 2017 We previously showed that the catechol-O-methyltransferase (COMT) genotype is related to the plasma level of morphine and the required dose of morphine in an exploratory prospective study. Morphine 143-151 catechol-O-methyltransferase Homo sapiens 30-58 28985716-3 2017 We previously showed that the catechol-O-methyltransferase (COMT) genotype is related to the plasma level of morphine and the required dose of morphine in an exploratory prospective study. Morphine 143-151 catechol-O-methyltransferase Homo sapiens 60-64 28985716-4 2017 The findings showed that a group of patients with a GG single nucleotide polymorphism (SNP) rs4680 in COMT required a significantly higher dose of morphine than a non-GG group. Morphine 147-155 catechol-O-methyltransferase Homo sapiens 102-106 28928973-2 2017 Previous studies indicate that a single nucleotide polymorphism in the catechol-O-methyltransferase (COMT) gene (rs4680; p.Val158Met) may present as a predictive biomarker for the response to morphine treatment. Morphine 192-200 catechol-O-methyltransferase Homo sapiens 71-99 28928973-2 2017 Previous studies indicate that a single nucleotide polymorphism in the catechol-O-methyltransferase (COMT) gene (rs4680; p.Val158Met) may present as a predictive biomarker for the response to morphine treatment. Morphine 192-200 catechol-O-methyltransferase Homo sapiens 101-105 28928973-8 2017 The required dose of morphine on day 1 was significantly higher for patients with the G/G genotype of COMT, compared with those with the A/A and A/G genotypes (P=0.013). Morphine 21-29 catechol-O-methyltransferase Homo sapiens 102-106 28928973-9 2017 The results of the present study provide additional evidence that the COMT genotype may be a predictive biomarker for the response to morphine treatment. Morphine 134-142 catechol-O-methyltransferase Homo sapiens 70-74 28084056-9 2017 However, results suggest that genetic variants in the COMT and OPRM1 irrespective of gender, and OPRD1 in males may contribute to the variability in morphine analgesia in experimental pain models. Morphine 149-157 catechol-O-methyltransferase Homo sapiens 54-58 28084056-2 2017 The aim of this study was to investigate whether genetic variants of mu-, kappa- and delta-opioid receptor genes (OPRM1, OPRK1 and OPRD1) and catechol-O-methyltransferase gene (COMT) are associated with the morphine analgesia. Morphine 207-215 catechol-O-methyltransferase Homo sapiens 142-170 28084056-2 2017 The aim of this study was to investigate whether genetic variants of mu-, kappa- and delta-opioid receptor genes (OPRM1, OPRK1 and OPRD1) and catechol-O-methyltransferase gene (COMT) are associated with the morphine analgesia. Morphine 207-215 catechol-O-methyltransferase Homo sapiens 177-181 28084056-6 2017 Variability in morphine analgesia to contact heat stimulation was associated with COMT rs4680 (p = 0.04), and rectal thermal stimulation was associated with OPRM1 rs9479757 (p = 0.03). Morphine 15-23 catechol-O-methyltransferase Homo sapiens 82-86 27288213-0 2016 Association of the OPRM1 and COMT genes" polymorphisms with the efficacy of morphine in Tunisian cancer patients: Impact of the high genetic heterogeneity in Tunisia? Morphine 76-84 catechol-O-methyltransferase Homo sapiens 29-33 25963335-5 2016 Statistically significant associations were found between COMT rs4633 and rs4680 genotypes and the amount of morphine self-administered through a patient-controlled analgesia pump. Morphine 109-117 catechol-O-methyltransferase Homo sapiens 58-62 26902643-9 2016 Combinations of genetic variants within OPRM1, COMT, and ESR1 better explain variability in morphine consumption than single genetic variants. Morphine 92-100 catechol-O-methyltransferase Homo sapiens 47-51 21127283-0 2011 Combined catechol-O-methyltransferase and mu-opioid receptor gene polymorphisms affect morphine postoperative analgesia and central side effects. Morphine 87-95 catechol-O-methyltransferase Homo sapiens 9-37 23686330-0 2013 Genetic variability at COMT but not at OPRM1 and UGT2B7 loci modulates morphine analgesic response in acute postoperative pain. Morphine 71-79 catechol-O-methyltransferase Homo sapiens 23-27 23686330-2 2013 METHODS: A total of 109 patients treated with morphine were genotyped by DNA sequencing for 12 DNA polymorphisms of the COMT, OPRM1 and UGT2B7 genes. Morphine 46-54 catechol-O-methyltransferase Homo sapiens 120-124 23686330-4 2013 RESULTS: An association between average morphine consumption during the first 24 postoperative hours by patient-controlled analgesia (PCA) and COMT haplotypes was found. Morphine 40-48 catechol-O-methyltransferase Homo sapiens 143-147 23686330-10 2013 CONCLUSIONS: By considering COMT, OPRM1, and UGT2B7 genotypes, as well as pharmacokinetic results, only COMT polymorphisms appear to be predictive of morphine need in postoperative pain therapy. Morphine 150-158 catechol-O-methyltransferase Homo sapiens 104-108 23210659-0 2013 The Val158Met polymorphism of the COMT gene is associated with increased pain sensitivity in morphine-treated patients undergoing a painful procedure after cardiac surgery. Morphine 93-101 catechol-O-methyltransferase Homo sapiens 34-38 23210659-2 2013 The relevance of these findings in morphine-treated postoperative cardiac patients undergoing painful healthcare procedures is unknown; therefore, the aim of this study was to investigate whether the COMT Val158Met polymorphism increases pain sensitivity in morphine-treated patients undergoing an unavoidable painful routine procedure after cardiac surgery. Morphine 258-266 catechol-O-methyltransferase Homo sapiens 200-204 23210659-9 2013 CONCLUSIONS: Our results show that the COMT Val158Met polymorphism contributes to variability in pain sensitivity after cardiac surgery of morphine-treated patients in the intensive care unit, because Met-allele carriers were more sensitive to overall pain and procedure-related pain. Morphine 139-147 catechol-O-methyltransferase Homo sapiens 39-43 26678969-5 2015 RESULTS: In patients with cancer-related pain, genetic variation in OPRM1, COMT, and ABCB1 is associated with response to morphine, which is the most well-studied opioid. Morphine 122-130 catechol-O-methyltransferase Homo sapiens 75-79 25155931-0 2014 Rescue morphine in mechanically ventilated newborns associated with combined OPRM1 and COMT genotype. Morphine 7-15 catechol-O-methyltransferase Homo sapiens 87-91 25155931-3 2014 RESULTS: For OPRM1 and COMT separately, the expected risk for rescue morphine or morphine dose was not significantly increased. Morphine 69-77 catechol-O-methyltransferase Homo sapiens 23-27 25155931-3 2014 RESULTS: For OPRM1 and COMT separately, the expected risk for rescue morphine or morphine dose was not significantly increased. Morphine 81-89 catechol-O-methyltransferase Homo sapiens 23-27 25155931-6 2014 CONCLUSION: Combined OPRM1 118A>G and COMT 472G>A genotype might serve as a predictor for the need of rescue morphine in premature and term newborns on mechanical ventilation. Morphine 115-123 catechol-O-methyltransferase Homo sapiens 41-45 24533707-10 2014 CONCLUSION: COMT SNPs may play a significant role in interindividual variation in postoperative pain perception and postoperative morphine requirements in children. Morphine 130-138 catechol-O-methyltransferase Homo sapiens 12-16 23773341-0 2013 An opposite-direction modulation of the COMT Val158Met polymorphism on the clinical response to intrathecal morphine and triptans. Morphine 108-116 catechol-O-methyltransferase Homo sapiens 40-44 23773341-2 2013 In the present study, we first evaluated the association between COMT rs4680 and the analgesic response to intrathecal morphine in patients with chronic low back pain to provide confirmation of previously reported positive findings. Morphine 119-127 catechol-O-methyltransferase Homo sapiens 65-69 23773341-4 2013 In patients with chronic low back pain (n = 74), logistic stepwise regression analysis showed that age (odds ratio [OR]: .90, 95% confidence interval [CI]: .85-.96, P = .002) and the presence of the COMT Met allele (vs Val/Val, OR: .21, 95% CI: .04-.98, P = .048) were predictive factors for lower risk of poor analgesic response to intrathecal morphine. Morphine 345-353 catechol-O-methyltransferase Homo sapiens 199-203 22293824-0 2012 Expression changes in arrestin beta 1 and genetic variation in catechol-O-methyltransferase are biomarkers for the response to morphine treatment in cancer patients. Morphine 139-147 catechol-O-methyltransferase Homo sapiens 63-91 22293824-7 2012 No correlation was observed between the genotype of OPRM1 and morphine treatment; however, the plasma concentration of morphine and the required dose of morphine were significantly lower for the A/A genotype of COMT (vs. A/G+G/G, P=0.008 and 0.03). Morphine 74-82 catechol-O-methyltransferase Homo sapiens 235-239 22293824-7 2012 No correlation was observed between the genotype of OPRM1 and morphine treatment; however, the plasma concentration of morphine and the required dose of morphine were significantly lower for the A/A genotype of COMT (vs. A/G+G/G, P=0.008 and 0.03). Morphine 131-139 catechol-O-methyltransferase Homo sapiens 235-239 22293824-7 2012 No correlation was observed between the genotype of OPRM1 and morphine treatment; however, the plasma concentration of morphine and the required dose of morphine were significantly lower for the A/A genotype of COMT (vs. A/G+G/G, P=0.008 and 0.03). Morphine 131-139 catechol-O-methyltransferase Homo sapiens 235-239 22293824-8 2012 We found that changes in the expression of ARRB1 may be a novel pharmacodynamic biomarker and the COMT 472G A genotype may be a predictive biomarker of the response to morphine treatment. Morphine 192-200 catechol-O-methyltransferase Homo sapiens 110-114 21127283-3 2011 In this study, we investigated whether combined catechol-O-methyltransferase and mu-opioid receptor polymorphisms contribute to the morphine response in postoperative analgesia. Morphine 132-140 catechol-O-methyltransferase Homo sapiens 48-76 21127283-8 2011 RESULTS: The heterozygous patients with mu-opioid receptor A118G and catechol-O-methyltransferase G1947A mutation consumed significantly less morphine in the postanesthetic recovery room and 48 hours after surgery compared with homozygous patients of the A118 variant. Morphine 142-150 catechol-O-methyltransferase Homo sapiens 69-97