Tobacco and estrogen metabolic polymorphisms and risk of non-small cell lung cancer in women

被引:72
作者
Cote, Michele L. [1 ,2 ]
Yoo, Wonsuk [2 ]
Wenzlaff, Angela S. [1 ]
Prysak, Geoffrey M. [1 ]
Santer, Susan K. [1 ]
Claeys, Gina B. [1 ]
Van Dyke, Alison L. [1 ,3 ]
Land, Susan J. [4 ,5 ]
Schwartz, Ann G. [1 ,2 ]
机构
[1] Karmanos Canc Inst, Populat Studies & Prevent Program, Detroit, MI 48201 USA
[2] Wayne State Univ, Sch Med, Dept Internal Med, Detroit, MI 48201 USA
[3] Wayne State Univ, Sch Med, Canc Biol Program, Detroit, MI 48201 USA
[4] Wayne State Univ, Sch Med, Dept Obstet & Gynecol, Appl Genom Technol Ctr, Detroit, MI 48201 USA
[5] Karmanos Canc Inst, Mol Biol & Genet Program, Detroit, MI 48201 USA
基金
美国国家卫生研究院;
关键词
CATECHOL-O-METHYLTRANSFERASE; TETRANUCLEOTIDE REPEAT POLYMORPHISM; HUMAN AROMATASE CYTOCHROME-P-450; RECEPTOR-BETA; ENDOMETRIAL CANCER; NEVER SMOKERS; REPRODUCTIVE FACTORS; STEROID-RECEPTORS; GENETIC-VARIATION; PREDICTION MODEL;
D O I
10.1093/carcin/bgp033
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
To explore the potential role for estrogen in lung cancer susceptibility, candidate single-nucleotide polymorphism (SNPs) in tobacco and estrogen metabolism genes were evaluated. Population-based cases (n = 504) included women aged 18-74, diagnosed with NSCLC in metropolitan Detroit between November 2001 and October 2005. Population-based controls (n = 527) were identified through random digit dialing and matched on race and age. Eleven SNPs in 10 different genes were examined in relation to risk: CYP1A1 Msp1, CYP1A1 Ile(462)Val, CYP1B1 Leu(432)Val, CYP17, CYP19A1, XRCC1 Gln(399)Arg, COMT Val(158)Met, NQO1 Pro(187)Ser, GSTM1, GSTT1 and GSTP1 Ile(105)Val. Lung cancer risk associated with individual SNPs was seen for GSTP1 [A allele; odds ratio (OR) = 1.85; 95% confidence interval (CI), 1.04-3.27] and XRCC1 (A/A genotype; OR = 1.68; 95% CI, 1.01-2.79) in white women and CYP1B1 (G allele; OR = 11.1; 95% CI, 1.18-104) in black women smokers. White women smokers carrying two risk genotypes at the following loci were at increased risk of lung cancer compared with individuals not carrying risk alleles at these loci: CYP17 and GSTM1, COMT and GSTM1, CYP17 and GSTT1, XRCC1 and GSTP1, CYP1B1 and XRCC1 and COMT and XRCC1. The most parsimonious model of lung cancer risk in white smoking women included age, family history of lung cancer, history of chronic lung disease, pack-years, body mass index, XRCC1 A/A genotype, GSTM1 null and COMT A/G or G/G genotype. These findings support the need for continued study of estrogen in relation to lung cancer risk. Polymorphisms in the tobacco metabolism, estrogen metabolism and DNA repair pathways will be useful in developing more predictive models of individual risk.
引用
收藏
页码:626 / 635
页数:10
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