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Carcinogenesis Advance Access published online on January 27, 2009
Carcinogenesis, doi:10.1093/carcin/bgp033
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© The Author 2009. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

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

Michele L. Cote1,2, Wonsuk Yoo2, Angela S. Wenzlaff1, Geoffrey M. Prysak1, Susan Santer1, Gina B. Claeys1, Alison L. VanDyke1,3, Susan J. Land4,5 and Ann G. Schwartz1,2

1 Population Studies and Prevention Program, Karmanos Cancer Institute
2 Department of Internal Medicine, Wayne State University School of Medicine
3 Cancer Biology Program, Wayne State University School of Medicine
4 Applied Genomics Technology Center, OB/GYN, Wayne State University School of Medicine
5 Molecular Biology and Genetics Program, Karmanos Cancer Institute

Reprint requests: Michele Cote, PhD, Karmanos Cancer Institute, 110 E. Warren Ave., Detroit, MI 48201. Phone: 313-578-4204. Fax: 313-578-4306. E-mail: cotem{at}karmanos.org.

To explore the potential role for estrogen in lung cancer susceptibility, candidate 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 Ile462Val, CYP1B1 Leu432Val, CYP17, CYP19A1, XRCC1 Gln399Arg, COMT Val158Met, NQO1 Pro187Ser, GSTM1, GSTT1, and GSTP1 Ile105Val. Lung cancer risk associated with individual SNPs was seen for GSTP1 (A allele; OR = 1.85; 95% 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 to 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, BMI, 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.

Key Words: lung cancer • epidemiology • cigarette smoking • Blacks • candidate gene

This research was funded by NIH grants R01-CA87895 and contracts N01-PC35145 and P30CA22453.

Received August 20, 2008; revised January 20, 2009; accepted January 20, 2009.


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