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Table 1 Association between smoking behaviour and nicotine dependence and ANKK1 / DRD2 Taq IA, SLC6A3 VNTR, and CYP2A6 polymorphisms

From: Genetic influence of dopamine receptor, dopamine transporter, and nicotine metabolism on smoking cessation and nicotine dependence in a Japanese population

Study Ethnicity Samples Association Reference
ANKK1 / DRD2 Taq IA polymorphism
Noble et al. (1994) Caucasians 57 current smokers, 115 former smokers, and 182 non-smokers Smoking subjects showed a significantly higher prevalence of the A1 allele compared to controls. Both past and current smokers demonstrated a significantly higher prevalence of the A1 allele than non-smokers did. [4]
Comings et al. (1996) Caucasians 312 smokers There was a significant, inverse relationship between the prevalence of the A1 allele and the age of onset of smoking, and the maximum duration of time that smokers had been able to quit smoking on their own. [5]
Batra et al. (2000) Caucasians 110 heavy smokers and 60 light smokers No significant findings [22]
Bierut et al. (2000) Caucasians 388 habitual smokers and 566 non-habitual smokers No significant findings [23]
Yoshida et al. (2001) Japanese 77 current smokers, 57 former smokers, and 198 never smokers Smoking appeared to be associated with the A2/A2 genotype. [6]
Hamajima et al, (2002) Japanese 226 current smokers, 133 former smokers, and 434 never smokers Males with the A2/A2 genotype had a higher risk of being current smokers. [7]
Johnstone et al. (2004) Caucasians 752 smokers At 1 week, the nicotine patch was more effective for smokers with the A1/A2 or A1/A1 genotypes than for those with the A2/A2 genotype; this was not the case at the 12-week flow up. [24]
Morton et al. (2006) Caucasians 1068 smokers, 213 non-smoking, and 1093 former smokers Current smokers were more likely than former smokers to possess the A1 allele. [25]
Connor et al. (2007) Caucasians 84 smokers Compared to carriers of the A2/A2 genotype, carriers of the A1/A1 or A1/A2 genotypes were characterised by higher levels of cigarette consumption. [26]
SLC6A3 VNTR polymorphism
Lerman et al. (1999) Caucasians (85%) African Americans (15%) 289 smokers and 233 non-smokers Individuals with the 9r allele were significantly less likely to be smokers, particularly if they also carried the A2/A2 genotype. Smokers carrying the 9r allele genotype were also significantly less likely to have started smoking before 16 years of age and had prior smoking histories, indicating a longer period of prior smoking cessation. [10]
Sabol et al. (1999) Caucasians 164 current smokers and 111 former smokers The 9r allele was associated with smoking cessation. [11]
Jorm et al. (2000) Caucasians 211 former smokers, 198 current smokers, and 452 non-smokers No associations were found with either smoking initiation or smoking cessation. [12]
Vandenbergh et al. (2002) Caucasians 153 former smokers, 98 current smokers, 214 never smokers, and 114 non-smokers Never smokers showed a higher prevalence of the 10r allele compared to current smokers. The frequency of the 10r allele in never-smokers (no cigarettes ever) was more than that in other smokers. [13]
Perkins et al. (2008) Caucasians 72 smoker The increase in smoking amount owing to negative mood was associated with the A2/A2 allele and the 9r allele. [17]
Laucht et al. (2008) Caucasians 220 ever smokers (adolescents) The A1 allele scored higher on nicotine dependence than their allelic counterparts. The intention to quit smoking was significantly lower in adolescents for the 10r/10r genotype. [27]
Sieminska et al. (2009) Caucasians 150 ever smokers and 158 never smokers The abstinence periods during quitting attempts of carriers of the A1 allele were longer than those of non-carriers. The odds ratio for heavy smoking was higher in carriers of the A1 or 9r alleles compared to that in non-carriers. Compared to non-carriers, carriers of the 9r allele had a lower risk to start smoking before the age of 20 years. [14]
CYP2A6 polymorphism (*4 allele)
Tan et al. (2001) Chinese 174 smokers and 152 non-smokers The distribution of the CYP2A6 genotype frequencies was not significantly different. [28]
Loriot et al. (2001) Caucasians 185 heavy smokers and 203 light smokers No significant relationship between genetically impaired nicotine metabolism and cigarette consumption related and the presence of defective CYP2A6 alleles (*2 and *4 alleles). [29]
Ando et al. ( 2003) Japanese 57 current smokers, 44 former smokers, and 139 never smokers The proportion of never smokers among heterozygous carriers of the *4 allele was similar among subjects with the *1/*1 genotype. CYP2A6 genotypes did not correlate either with the number of cigarettes smoked per day or with the age of smoking commencement. [30]
Minematsu et al. (2003) Japanese 92 current smokers, 111 former smokers, and 123 non-smoker The percentage of subjects with a CYP2A6del (*4) allele was lower among heavy smokers than among light smokers or non-smokers and was lower among ex-smokers than among current smokers. [20]
Fujieda et al. (2004) Japanese 1094 patient (cancer) subjects and 611 healthy subjects The amount of daily cigarette consumption in subjects who harboured the CYP2A6*4 allele was significantly less than that in subjects carrying the *1/*1 genotype. [31]
Kubota et al. (2006) Japanese 107 smokers CYP2A6 high-activity group (CYP2A6*1/*1, *1/*4, etc.) smoked the first cigarette of the day earlier than the low-activity group (CYP2A6*4/*4), indicating more marked nicotine dependence. Nicotine withdrawal symptoms were more serious during smoking cessation in the CYP2A6 high-activity group. [21]
Liu et al. (2011) Chinese 970 current smokers and 358 former smokers Poor metabolizers reported smoking fewer cigarettes per day, started smoking regularly at a later age, and smoked for a shorter duration than did normal metabolizers. However, poor metabolizers were less likely to quit smoking than normal metabolizers were. [32]