PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 34895312-12 2021 Finally, we captured a DNA methylation signature associated with COPD diagnosis in a gene involved in nicotine dependence (COMT) (FDR < 0.1, Deltabeta > 0.05). Nicotine 102-110 catechol-O-methyltransferase Homo sapiens 123-127 15900212-2 2005 To determine if the lower activity Met allele of COMT was associated with smoking cessation in women, we used two independent studies: a population-based case--control study and a nicotine replacement clinical trial. Nicotine 180-188 catechol-O-methyltransferase Homo sapiens 49-53 16395295-0 2006 Significant association of catechol-O-methyltransferase (COMT) haplotypes with nicotine dependence in male and female smokers of two ethnic populations. Nicotine 79-87 catechol-O-methyltransferase Homo sapiens 27-55 16395295-0 2006 Significant association of catechol-O-methyltransferase (COMT) haplotypes with nicotine dependence in male and female smokers of two ethnic populations. Nicotine 79-87 catechol-O-methyltransferase Homo sapiens 57-61 16395295-2 2006 Allelic variants within the COMT gene are therefore potential candidates for examining interindividual differences in vulnerability to nicotine dependence (ND). Nicotine 135-143 catechol-O-methyltransferase Homo sapiens 28-32 16395295-8 2006 Further examination of two protective haplotypes, A-G-T in AAs and T-G-T in EAs, indicated that the low COMT enzyme activity Met allele is protective to become nicotine dependent. Nicotine 160-168 catechol-O-methyltransferase Homo sapiens 104-108 26555332-0 2015 Association between catechol-O-methyltransferase (COMT) Val/Met genotype and smoking cessation treatment with nicotine: a meta-analysis. Nicotine 110-118 catechol-O-methyltransferase Homo sapiens 20-48 26555332-0 2015 Association between catechol-O-methyltransferase (COMT) Val/Met genotype and smoking cessation treatment with nicotine: a meta-analysis. Nicotine 110-118 catechol-O-methyltransferase Homo sapiens 50-54 26555332-1 2015 AIM: Catechol-O-methyltransferase (COMT) is one of the major degradative pathways of dopamine and COMT Val/Met polymorphisms are associated with the enzyme activity, which is related to dopamine involvement in the nicotine addiction process. Nicotine 214-222 catechol-O-methyltransferase Homo sapiens 5-33 26555332-1 2015 AIM: Catechol-O-methyltransferase (COMT) is one of the major degradative pathways of dopamine and COMT Val/Met polymorphisms are associated with the enzyme activity, which is related to dopamine involvement in the nicotine addiction process. Nicotine 214-222 catechol-O-methyltransferase Homo sapiens 35-39 26555332-1 2015 AIM: Catechol-O-methyltransferase (COMT) is one of the major degradative pathways of dopamine and COMT Val/Met polymorphisms are associated with the enzyme activity, which is related to dopamine involvement in the nicotine addiction process. Nicotine 214-222 catechol-O-methyltransferase Homo sapiens 98-102 26555332-8 2015 CONCLUSION: The COMT polymorphisms are associated with the outcomes following smoking cessation treatment with nicotine. Nicotine 111-119 catechol-O-methyltransferase Homo sapiens 16-20 22695756-0 2012 Association of functional COMT Val108/Met polymorphism with smoking cessation in a nicotine replacement therapy. Nicotine 83-91 catechol-O-methyltransferase Homo sapiens 26-30 26096691-0 2015 COMT polymorphism modulates the resting-state EEG alpha oscillatory response to acute nicotine in male non-smokers. Nicotine 86-94 catechol-O-methyltransferase Homo sapiens 0-4 26096691-2 2015 As individual difference in response to nicotine may be related to a functional polymorphism in the gene encoding catechol-O-methyltransferase (COMT), an enzyme that strongly influences cortical dopamine metabolism, this study examined the modulatory effects of the COMT Val158Met polymorphism on the neural response to acute nicotine as measured with resting-state electroencephalographic (EEG) oscillations. Nicotine 40-48 catechol-O-methyltransferase Homo sapiens 114-142 26096691-2 2015 As individual difference in response to nicotine may be related to a functional polymorphism in the gene encoding catechol-O-methyltransferase (COMT), an enzyme that strongly influences cortical dopamine metabolism, this study examined the modulatory effects of the COMT Val158Met polymorphism on the neural response to acute nicotine as measured with resting-state electroencephalographic (EEG) oscillations. Nicotine 40-48 catechol-O-methyltransferase Homo sapiens 144-148 26096691-2 2015 As individual difference in response to nicotine may be related to a functional polymorphism in the gene encoding catechol-O-methyltransferase (COMT), an enzyme that strongly influences cortical dopamine metabolism, this study examined the modulatory effects of the COMT Val158Met polymorphism on the neural response to acute nicotine as measured with resting-state electroencephalographic (EEG) oscillations. Nicotine 40-48 catechol-O-methyltransferase Homo sapiens 266-270 26096691-2 2015 As individual difference in response to nicotine may be related to a functional polymorphism in the gene encoding catechol-O-methyltransferase (COMT), an enzyme that strongly influences cortical dopamine metabolism, this study examined the modulatory effects of the COMT Val158Met polymorphism on the neural response to acute nicotine as measured with resting-state electroencephalographic (EEG) oscillations. Nicotine 326-334 catechol-O-methyltransferase Homo sapiens 144-148 23459442-0 2013 COMT Val158Met modulates subjective responses to intravenous nicotine and cognitive performance in abstinent smokers. Nicotine 61-69 catechol-O-methyltransferase Homo sapiens 0-4 23459442-1 2013 The catechol-O-methyltransferase (COMT) Val158Met polymorphism may be a risk factor for nicotine addiction. Nicotine 88-96 catechol-O-methyltransferase Homo sapiens 4-32 23459442-1 2013 The catechol-O-methyltransferase (COMT) Val158Met polymorphism may be a risk factor for nicotine addiction. Nicotine 88-96 catechol-O-methyltransferase Homo sapiens 34-38 23828159-1 2013 RATIONALE: The common methionine (met) for valine (val) at codon 158 (val(158)met) polymorphism in the catechol-O-methyltransferase (COMT) gene has been associated with nicotine dependence, alterations in executive cognitive function, and abstinence-induced working memory deficits in smokers. Nicotine 169-177 catechol-O-methyltransferase Homo sapiens 103-131 23828159-1 2013 RATIONALE: The common methionine (met) for valine (val) at codon 158 (val(158)met) polymorphism in the catechol-O-methyltransferase (COMT) gene has been associated with nicotine dependence, alterations in executive cognitive function, and abstinence-induced working memory deficits in smokers. Nicotine 169-177 catechol-O-methyltransferase Homo sapiens 133-137 23433232-1 2013 Nicotine and tonic dopamine (DA) levels [as inferred by catechol-O-methyl tranferase (COMT) Val158Met genotype] interact to affect prefrontal processing. Nicotine 0-8 catechol-O-methyltransferase Homo sapiens 56-84 23433232-1 2013 Nicotine and tonic dopamine (DA) levels [as inferred by catechol-O-methyl tranferase (COMT) Val158Met genotype] interact to affect prefrontal processing. Nicotine 0-8 catechol-O-methyltransferase Homo sapiens 86-90 23433232-5 2013 A significant nicotine x COMT genotype interaction for BOLD signal during performance feedback in cortico-striatal areas was seen. Nicotine 14-22 catechol-O-methyltransferase Homo sapiens 25-29 23433232-10 2013 Although these results are preliminary due to small sample size, they suggest a possible neurobiological mechanism underlying the clinical observation that Val/Val homozygotes, presumably with elevated COMT activity compared to Met allele carriers and therefore reduced prefrontal DA levels, have poorer outcomes with nicotine replacement therapy. Nicotine 318-326 catechol-O-methyltransferase Homo sapiens 202-206 21423427-1 2010 We previously reported that catechol-O-methyltransferase (COMT) is significantly associated with nicotine dependence (ND) in humans. Nicotine 97-105 catechol-O-methyltransferase Homo sapiens 28-56 21312287-1 2010 VII COMT as a risk modifying gene for Nicotine dependence - role of gene-gene interaction, personality, and environmental factors. Nicotine 38-46 catechol-O-methyltransferase Homo sapiens 4-8 21312287-2 2010 OBJECTIVES: Catechol-O-methyltransferase (COMT) may be a risk modifying gene for Nicotine dependence (ND) rather than a direct susceptibility gene for this phenotype. Nicotine 81-89 catechol-O-methyltransferase Homo sapiens 12-40 21312287-2 2010 OBJECTIVES: Catechol-O-methyltransferase (COMT) may be a risk modifying gene for Nicotine dependence (ND) rather than a direct susceptibility gene for this phenotype. Nicotine 81-89 catechol-O-methyltransferase Homo sapiens 42-46 20712524-1 2010 AIMS: This study evaluates the relationship of six polymorphisms found in the CHRNA3, DRD2 and COMT genes with nicotine dependence, the ability to quit smoking and the occurrence of withdrawal symptoms after short-term use of nicotine patch in hospitalized patients. Nicotine 111-119 catechol-O-methyltransferase Homo sapiens 95-99 20712524-1 2010 AIMS: This study evaluates the relationship of six polymorphisms found in the CHRNA3, DRD2 and COMT genes with nicotine dependence, the ability to quit smoking and the occurrence of withdrawal symptoms after short-term use of nicotine patch in hospitalized patients. Nicotine 226-234 catechol-O-methyltransferase Homo sapiens 95-99 21492092-9 2011 Individuals possessing a paucity of serotonergic and/or dopaminergic receptors and an increased rate of synaptic dopamine catabolism, due to high catabolic genotype of the COMT gene, are predisposed to self-medicating any substance or behavior that will activate dopamine release including alcohol, opiates, psychostimulants, nicotine, glucose, gambling, sex, and even excessive internet gaming, among others. Nicotine 326-334 catechol-O-methyltransferase Homo sapiens 172-176 21423427-1 2010 We previously reported that catechol-O-methyltransferase (COMT) is significantly associated with nicotine dependence (ND) in humans. Nicotine 97-105 catechol-O-methyltransferase Homo sapiens 58-62 17548664-3 2007 The genotype x treatment interaction effect at 12-week follow-up indicated a greater benefit of active nicotine replacement treatment compared with placebo on likelihood of abstinence in the COMT Met/Met genotype group (33% versus 12%), in comparison to the Met/Val + Val/Val group (22% versus 16%). Nicotine 103-111 catechol-O-methyltransferase Homo sapiens 191-195 19065145-1 2009 The val allele of the catechol-O-methyltransferase (COMT) val(158)met polymorphism has been linked with nicotine dependence and with cognitive performance in healthy volunteers. Nicotine 104-112 catechol-O-methyltransferase Homo sapiens 22-50 19065145-1 2009 The val allele of the catechol-O-methyltransferase (COMT) val(158)met polymorphism has been linked with nicotine dependence and with cognitive performance in healthy volunteers. Nicotine 104-112 catechol-O-methyltransferase Homo sapiens 52-56 19065145-7 2009 These data suggest a novel brain-behavior mechanism that may underlie the increased susceptibility to nicotine dependence and smoking relapse associated with the COMT val allele. Nicotine 102-110 catechol-O-methyltransferase Homo sapiens 162-166 18192898-1 2008 OBJECTIVES: We attempted to extend a previous finding of an association of COMT genotype with response to nicotine-replacement therapy (NRT), in a larger cohort of treatment-seeking smokers, with greater statistical power to detect possible moderating effects of sex. Nicotine 106-114 catechol-O-methyltransferase Homo sapiens 75-79 20188797-8 2010 These results suggest that carriers of the high activity COMT variant are more prone to develop a higher level of nicotine dependence, or that they release more dopamine than carriers of Met/Met or Met/Val genotypes. Nicotine 114-122 catechol-O-methyltransferase Homo sapiens 57-61 19014506-4 2008 Individuals possessing a paucity of serotonergic and/or dopaminergic receptors, and an increased rate of synaptic DA catabolism due to high catabolic genotype of the COMT gene, are predisposed to self-medicating any substance or behavior that will activate DA release, including alcohol, opiates, psychostimulants, nicotine, gambling, sex, and even excessive internet gaming. Nicotine 315-323 catechol-O-methyltransferase Homo sapiens 166-170 17548664-0 2007 Association of COMT Val108/158Met genotype with smoking cessation in a nicotine replacement therapy randomized trial. Nicotine 71-79 catechol-O-methyltransferase Homo sapiens 15-19 17548664-4 2007 Our results indicate that COMT genotype may moderate the effect of active transdermal nicotine patch compared with placebo, with reduced relative benefit of nicotine replacement therapy in individuals with Met/Val or Val/Val genotype. Nicotine 86-94 catechol-O-methyltransferase Homo sapiens 26-30