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Carcinogenesis Advance Access published online on January 10, 2008
Carcinogenesis, 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,#, Guangfu Jin2,#, 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, Texas 77030, USA

* To whom correspondence and reprints should be addressed. E-mail: drlu{at}fudan.edu.cn

** Correspondence may also be addressed to 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 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.

# 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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