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Carcinogenesis Advance Access published online on November 25, 2004
Carcinogenesis, doi:10.1093/carcin/bgh343
© 2004 by Oxford University Press
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Received July 7, 2004
Revised October 18, 2004
Accepted November 17, 2004

MOLECULAR EPIDEMIOLOGY AND CANCER PREVENTION

The PPAR{gamma} Pro12Ala polymorphism and risk for incident sporadic colorectal adenomas

Zhihong Gong 1, Dawen Xie 1*, Zonglin Deng 1, Roberd M. Bostick 2, Stephanie J. Muga 3, Thomas G. Hurley 1, and James R. Hebert 4

1 Department of Epidemiology and Biostatistics, University of South Carolina, Arnold School of Public Health, Columbia, SC; South Carolina Cancer Center, Columbia, SC
2 Department of Epidemiology, Rollins School of Public Health, Emory University, Atlanta, GA
3 South Carolina Cancer Center, Columbia, SC; Department of Pathology, University of South Carolina School of Medicine, Columbia, SC
4 Department of Epidemiology and Biostatistics, University of South Carolina, Arnold School of Public Health, Columbia, SC; South Carolina Cancer Center, Columbia, SC; Hollings Cancer Center, Medical University of South Carolina, Charleston, SC

* To whom correspondence should be addressed.
Dawen Xie, E-mail: dawen.xie{at}PalmettoHealth.org


  Abstract

Peroxisome proliferator-activated receptor {gamma}(PPAR{gamma}), a member of the nuclear hormone receptor superfamily initially shown to be a key regulator of fat cell differentiation, can inhibit cell growth and induce apoptosis in colon cell lines. There are heterozygous loss-of-function mutations in the gene encoding PPAR{gamma} in tumors from {approx}10% of human colon cancer patients. A common structural polymorphism has been detected in the PPAR{gamma} gene at codon 12 (Pro12Ala). We investigated the hypothesis that the PPAR{gamma} Pro12Ala polymorphism is associated with colorectal adenoma risk in a recently concluded case-control study of incident sporadic colorectal adenomas (163 cases and 212 controls). The multivariate-adjusted odds ratio (OR) for incident sporadic colorectal adenoma was 0.65 (95% CI: 0.39-1.09) for those with Pro12Ala or Ala12Ala genotypes compared to those with the Pro12Pro genotype. Multivariate-adjusted inverse associations with the Ala12 variant were more pronounced among those who were female (OR: 0.36; 95% CI: 0.18-0.75) or did not take NSAIDs (OR: 0.38; 95% CI: 0.14-1.00). Marginally significant results were observed among those with a lower waist:hip ratio (OR: 0.52; 95% CI: 0.24-1.12) or a lower body mass index (OR: 0.46; 95%: 0.20-1.05). Smoking was a very strong risk factor (OR: 2.34; 95%CI: 1.37-4.02) for colorectal adenoma among those with wild type (Pro12Pro), but not those with the Ala12 variant (OR: 0.86; 95%CI: 0.35-2.09). Larger studies are needed to validate these results, which suggest that the PPAR{gamma} Pro12Ala polymorphism may interact with other factors to protect against colorectal adenoma.


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