| Literature DB >> 18187557 |
Dan Chen1, Guangfu Jin, Ying Wang, Haifeng Wang, Hongliang Liu, Yanhong Liu, Weiwei Fan, Hongxia Ma, Ruifeng Miao, Zhibin Hu, Weiwei Sun, Ji Qian, Li Jin, Qingyi Wei, Hongbing Shen, Wei Huang, Daru Lu.
Abstract
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.Entities:
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Year: 2008 PMID: 18187557 DOI: 10.1093/carcin/bgm285
Source DB: PubMed Journal: Carcinogenesis ISSN: 0143-3334 Impact factor: 4.944