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Carcinogenesis Advance Access originally published online on January 10, 2008
Carcinogenesis 2008 29(2):342-350; doi:10.1093/carcin/bgm285
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© The Author 2008. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Genetic variants in peroxisome proliferator-activated receptor-{gamma} gene are associated with risk of lung cancer in a Chinese population

Dan Chen1,{dagger}, Guangfu Jin2,{dagger}, Ying Wang3, Haifeng Wang3, Hongliang Liu1, Yanhong Liu1, Weiwei Fan1, Hongxia Ma2, Ruifeng Miao2, Zhibin Hu2, Weiwei Sun3, Ji Qian1, Li Jin1,3, Qingyi Wei4, Hongbing Shen2, Wei Huang3,* and Daru Lu1,*

1 The State Key Laboratory of Genetic Engineering and The MOE Key Laboratory of Contemporary Anthropology, School of Life Sciences, Fudan University, Shanghai 200433, China
2 Department of Epidemiology and Biostatistics, Cancer Research Center of Nanjing Medical University, Nanjing 210029, China
3 Department of Genetics, Shanghai-MOST Key Laboratory of Health and Disease Genomics, Chinese National Human Genome Center, Shanghai 201203, China
4 Department of Epidemiology, The University of Texas M. D. Anderson Cancer Center, Houston, TX 77030, USA

* To whom correspondence should be addressed. Tel/Fax: +86 21 65642799; Email: drlu{at}fudan.edu.cn Correspondence may also be addressed to Wei Huang. Tel: +86 21 50801795; Fax: +86 21 50801922; Email: huangwei{at}chgc.sh.cn

Accumulating evidence indicates that activation of the peroxisome proliferator-activated receptor-{gamma} (PPAR-{gamma}) dampens the inflammation cascade and inhibits tumor growth of the lung, suggesting that it has tumor suppressor functions. We performed a case–control study of 500 incident lung cancer cases and 517 age- and sex frequency-matched cancer-free controls in a Chinese population to investigate the role of 11 selected single nucleotide polymorphisms (SNPs) of PPAR-{gamma} in the etiology of lung cancer. We found that decreased lung cancer risk was statistically significantly associated with seven SNPs (P = 0.0004 for rs13073869 and 0.0130 for rs1899951 in a dominant model; P = 0.0310 for rs4135247 in a log-additive model; and P = 0.0468 for rs2972162, 0.0175 for rs709151, 0.0172 for rs11715541 and 0.0386 for rs1175543 in an overdominant model). Consistent with these results of single-locus analysis, both the haplotype and the diplotype analyses revealed a protective effect of the haplotype ‘AGA’ and ‘AAA’ of rs13073869, rs1899951 and rs4135247. Furthermore, we observed a statistically significant interaction between the rs1899951 and cigarette smoking. Our results indicate that PPAR-{gamma} polymorphisms and their interaction with smoking may contribute to the etiology of lung cancer. These findings need to be validated in larger, preferably population-based, studies including different ethnic groups.

Abbreviations: PPAR-{gamma}, peroxisome proliferator-activated receptor-{gamma}; SNP, single nucleotide polymorphism; OR, odds ratio; CI, confidence interval; MAF, minor allele frequency; LD, linkage disequilibrium; HWE, Hardy-Weinberg equilibrium

{dagger} The first two authors contributed equally to this work.

Received September 8, 2007; revised November 14, 2007; accepted December 1, 2007.


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