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Carcinogenesis Advance Access published online on September 29, 2005
Carcinogenesis, doi:10.1093/carcin/bgi227
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© The Author 2005. Published by Oxford University Press. All rights reserved. For permissions, please email: journals.permissions@oupjournals.org
Received June 8, 2005
Revised August 17, 2005
Accepted September 11, 2005

MOLECULAR EPIDEMIOLOGY AND CANCER PREVENTION

CYP1A1 Ile462Val and MPO G-463A interact to increase risk of adenocarcinoma but not squamous cell carcinoma of the lung

Jill Everland Larsen 1, Maree Louise Colosimo 2, Ian Anthony Yang 1, Rayleen Bowman 3, Paul Victor Zimmerman 1, and Kwun Meng Fong 1*

1 Department of Thoracic Medicine, The Prince Charles Hospital, Brisbane, Australia; School of Medicine, University of Queensland, Brisbane, Australia
2 Department of Thoracic Medicine, The Prince Charles Hospital, Brisbane, Australia
3 School of Medicine, University of Queensland, Brisbane, Australia

* To whom correspondence should be addressed.
Kwun Meng Fong, E-mail: kwun_fong{at}health.qld.gov.au


  Abstract

Common polymorphisms in genes encoding phase I and phase II enzymes are considered to modify lung cancer risk due to changes in enzyme activity. Candidates include genetic variants of glutathione S-transferases (GSTM1, GSTT1 and GSTP1) and myeloperoxidase (MPO). We performed a large case-control study of these candidate genes in 1,103 patients with non-small cell lung cancer (NSCLC) and 627 controls without NSCLC. Associations between deletion genotypes of GSTM1 and GSTT1 and between single nucleotide polymorphisms (SNPs) of GSTP1 Ile105Val and MPO G-463A were first tested by adjusted logistic regression. Then we analysed gene-gene interactions, also incorporating our published data on the Ile462Val SNP in the phase I enzyme, cytochrome P450 CYP1A1. The homozygous GSTP1 Ile105Val genotype was significantly under-represented in NSCLC compared with controls (OR=0.73; 95%CI 0.53-1.00; P=0.050) especially in females (OR=0.57; 95%CI 0.34-0.98; P=0.04). The GSTT1-null genotype was significantly over-represented in adenocarcinomas (OR=1.41; 95%CI 1.06-1.90; P=0.02) but not in squamous cell carcinomas (OR=1.03; 95%CI 0.76-1.41; P=0.84). There was weak risk reduction associated with GSTM1-null in heavier smokers (OR=0.71; 95%CI 0.54-0.94; P=0.02), but neither GSTM1 nor MPO genotypes affected the overall risk of NSCLC. The MPO and CYP1A1 risk genotypes interacted to increase overall risk of NSCLC (OR=2.88; 95%CI 1.70-5.00; P<0.001). The data are consistent with the concept that multiple genes of modest effect interact to confer genomic-based susceptibility to lung cancer.

Keywords: non-small cell lung carcinoma; glutathione S-transferases; myeloperoxidase; cytochrome P450 1A1.
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