A novel CYP1A1 gene polymorphism in African-Americans

Crofts, Frances; Cosma, Greg; Currie, Diane; Taioli, Emanuela; Toniolo, Paolo; Garte, Seymour

doi:10.1093/carcin/14.9.1729

Cited by 111 publications

(53 citation statements)

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“…Additionally, a third polymorphism in CYP1A1 that is unique to African Americans has also been identified. This polymorphism, located in intron 7 at base number 5996, results in a single A-T to G-C transition and does not appear to be linked to the other polymorphisms in CYP1A1 [14]. Evidence suggests that this polymorphism is not significantly associated with lung cancer in African Americans [15][16][17] [12,17] but findings in Caucasian populations have been mixed for both polymorphisms [18][19][20].…”

Section: Cyp1a1mentioning

confidence: 99%

Combinations of cytochrome P-450 genotypes and risk of early-onset lung cancer in Caucasians and African Americans: A population-based study

et al. 2007

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Polymorphisms in CYP1A1 and CYP1B1 genes in humans are associated with reduction of enzymatic activity towards several substrates, including those found in tobacco smoke. To investigate the potential role these polymorphisms have as modulators of early-onset lung cancer risk, a populationbased case-control study involving early-onset lung cancer cases was performed. Biological samples were available for 383 individuals diagnosed prior to 50 years of age identified from the metropolitan Detroit Surveillance, Epidemiology and End Results (SEER) program and 449 age, race and sexmatched controls ascertained through random digit dialing. Genotype frequencies varied significantly by race for CYP1A1 exon 7 Ile 462 Val and CYP1B1 Leu 432 Val genotypes, so all analyses were stratified by race. No association was seen between lung cancer risk and polymorphisms in CYP1A1 MspI or CYP1B1 Leu 432 Val for Caucasians or African Americans, after adjusting for age at diagnosis, sex, pack years of smoking and family history of lung cancer. In Caucasians, those with the Ile/Val genotype at CYP1A1 exon 7 locus were at decreased risk of having lung cancer compared to those with the Ile/Ile genotype, after adjusting for age at diagnosis, sex, pack years of smoking and family history of cancer (OR=0.41 95% CI 0.19-0.90). These results were not replicated among the African American population, nor were they modified by amount of smoking.

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Section: Cyp1a1mentioning

confidence: 99%

Combinations of cytochrome P-450 genotypes and risk of early-onset lung cancer in Caucasians and African Americans: A population-based study

et al. 2007

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“…Black smokers have higher blood levels of cotinine, the main metabolite of nicotine, than do whites smoking a similar number of cigarettes per day (King and Brunetta, 1999). Several genetic studies report that black smokers have a distinctive polymorphism of the CYP1A1 gene associated with adenocarcinoma of the lung compared to white smokers Crofts et al, 1993;London et al, 1999;Shields et al, 1993;Taioli et al, 1998). Consequently, the carcinogenic or mutagenic agents in tobacco smoke may be metabolized and excreted at different rates in blacks than in whites (King and Brunetta, 1999;Perez-Stable et al, 1998;Richie et al, 1997).…”

Section: Lung Cancer Risk In African Americans Versus Caucasiansmentioning

confidence: 99%

Tobacco use and cancer: an epidemiologic perspective for geneticists

2002

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Much of what is known about the deleterious effects of tobacco use on health was learned from epidemiologic studies over the last half century. These studies establish unequivocally that tobacco use, particularly manufactured cigarette smoking, causes most cancers of the lung, oropharynx, larynx, and esophagus in the USA, and approximately one-third of all cancers of the pancreas, kidney, urinary bladder and uterine cervix. More recent evidence also implicates smoking with cancers of the stomach, liver and colorectum. While over half of the estimated 440 000 smoking-attributable deaths that occur annually in the USA involve non-malignant cardiovascular and respiratory conditions, smoking-attributable cancers are more recognized and feared. Geneticists increasingly study tobacco use as a model for environmental carcinogenicity. Tobacco-exposed populations provide opportunities to characterize the somatic mutations that give rise to specific cancers and to identify the inherited genetic traits that confer susceptibility or resistance. Studies to identify the genetic determinants of addiction may be particularly important. Future research to identify other susceptibility factors, such as genes that modify carcinogen metabolism or DNA repair, will need to be substantially larger and to quantify lifetime tobacco exposure with more precision than have past studies in order to distinguish gradations in risk due to exposure from those caused by genetic susceptibility. This review considers: (a) the epidemiology of tobacco use; (b) cancers presently classified as smoking-attributable by the US Surgeon General; (c) the magnitude of the epidemic of cancers and other diseases caused by tobacco use; (d) selected issues in the epidemiology of lung cancer; and (e) the interface of genetics and epidemiology in understanding, preventing, and treating tobacco-attributable disease.

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“…Cosma et al (1993) found significantly elevated levels of inducible lymphocyte CYP1A1 enzyme activity in individuals carrying A2455G when compared to wild type genotypic individuals. Crofts et al (1993) reported a threefold elevation in CYP1A1 enzymatic activity associated with A2455G G/ G genotypes. The T3801C allele was also reported to encode an inducible form of CYP1A1 (Kiyohara et al 1996).…”

Section: Introductionmentioning

confidence: 98%

“…The 2-hydroxylation products (2-OH estradiol catechol and 2-OH estrone catechol) lack estrogenic activities (Kawajiri et al 1990). Furthermore, the 2-hydroxy catechol metabolites can be converted by Omethylation into 2-methoxy derivatives, which have been shown to possess anti-proliferative and anti-angiogenic properties (Cascorbi et al 1996;Crofts et al 1993). Another, mutually exclusive, pathway of estrogenic metabolism is 16a-hydroxylation, which produces strong estrogenic metabolites and had been linked to estrogeninduced carcinogenesis in both laboratory animals and humans (Cushman et al 1995;Fotsis et al 1994).…”

Section: Introductionmentioning

confidence: 99%

“…These contrasting functions make CYP1A1 an interesting candidate factor that might influence susceptibility to breast cancer risk. T3801C (a substitution in the 3¢ non-coding region; Spurr et al 1987), A2455G (isoleucine change to valine at codon 462; Hayashi et al 1991), T3205C (a transition mutation in the 3¢ non-coding region; Crofts et al 1993), C2453A (threonine to asparagine change at codon 461; Cascorbi et al 1996) are four polymorphisms that have been found in this gene. Among them, C2453A is very rare and T3205C exists only in Africans or AfricanAmericans, so most studies have focused on T3801C and A2455G.…”

Section: Introductionmentioning

confidence: 99%

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Cytochrome P450 1A1 (CYP1A1) T3801C and A2455G polymorphisms in breast cancer risk: a meta-analysis

Chen

Huang

et al. 2007

J Hum Genet

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The cytochrome P450 1A1 gene (CYP1A1), encoding Phase I metabolic enzymes, appeared to be a candidate gene for breast cancer risk. However, studies on the association between polymorphisms in this gene and breast cancer have yielded conflicting results. We performed a meta-analysis to investigate the association with breast cancer of the CYP1A1 polymorphisms T3801C (9,316 cases and 12,714 controls) and A2455G (9,552 cases and 9,320 controls). In the genotype contrast of A2455G, both additive [GG vs AA, P = 0.04, fixed-effects OR 0.72; 95% CI (0.53-0.99), P = 0.95 for heterogeneity] and recessive [GG vs (GA + AA), P = 0.04, fixed-effects OR 0.73; 95% CI (0.53-0.99), P = 0.97 for heterogeneity] models produced significant results in east-Asians. In premenopausal women in a worldwide population, significant association between A2455G and breast cancer was also found using both models [additive model: P = 0.02, fixedeffects OR 0.52; 95% CI (0.29-0.92), P = 0.39 for heterogeneity; recessive model: P = 0.02, fixed-effects OR 0.51; 95% CI (0.29-0.90), P = 0.38 for heterogeneity]. Our meta-analysis suggests that an A2455G G/G genotype is associated with a trend of reduced breast cancer risk, both in east-Asian women and in pre-menopausal women worldwide, while the T3801C C allele might not be a risk factor for breast cancer. Larger scale primary studies are required to further evaluate the interaction of CYP1A1 polymorphisms and breast cancer risk in specific populations.

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A novel CYP1A1 gene polymorphism in African-Americans

Cited by 111 publications

References 0 publications

Combinations of cytochrome P-450 genotypes and risk of early-onset lung cancer in Caucasians and African Americans: A population-based study

Combinations of cytochrome P-450 genotypes and risk of early-onset lung cancer in Caucasians and African Americans: A population-based study

Tobacco use and cancer: an epidemiologic perspective for geneticists

Cytochrome P450 1A1 (CYP1A1) T3801C and A2455G polymorphisms in breast cancer risk: a meta-analysis

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