Carcinogenesis Advance Access published online on January 18, 2007
Carcinogenesis, doi:10.1093/carcin/bgm002
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Trans Fatty Acid Intake and Increased Risk of Advanced Prostate Cancer: Modification by RNASEL R462Q Variant
1 Department of Epidemiology & Biostatistics and Institute for Human Genetics, University of California, San Francisco, San Francisco, California 94143-0794
2 Present address: Mary Ann J. Milburn Smith Child Health Research Program, Department of Pediatrics, Northwestern University Feinberg School of Medicine and Children's Memorial Hospital and Children's Memorial Research Center, Chicago, IL 60614
3 Channing Laboratory, Brigham and Women's Hospital and Department of Epidemiology, Harvard School of Public Health, Boston, MA
4 Department of Cancer Biology, Lerner Research Institute, The Cleveland Clinic, Cleveland, Ohio 44195
* Corresponding authors: John S. Witte, Department of Epidemiology & Biostatistics, Center for Human Genetics, University of California, San Francisco, San Francisco, California 94143-0794, Telephone: 415-502-6882, Fax: 415-476-1356, wittej{at}humgen.ucsf.edu; Xin Liu, Mary Ann J. Milburn Smith Child Health Research Program, Department of Pediatrics, Northwestern University Feinberg School of Medicine, Chicago, IL 60614, Telephone: 312-573-7751, Fax: 312-573-7825, lliu{at}childrensmemorial.org
Previous studies have examined the role of higher trans fatty acid consumption on prostate cancer risk, but the results remain unclear. Any potential association may be modified by variants in genes involved with immune and inflammatory responses. To investigate this, we undertook a case-control study (N=1,012) of the association between trans fatty acid intake and advanced prostate cancer, and evaluated whether this effect was modified by a functional polymorphism in the RNASEL gene (R462Q). Among Caucasians (N=834), we observed that each type of trans fatty acid and total trans fatty acid intake showed a statistically significant positive association with prostate cancer, but only weakly increased risk for the isomers of cis fatty acids. Compared to the lowest quartile of total trans fatty acid consumption, the higher quartiles gave odds ratios (ORs) equal to 1.58 (95% CI: 1.00, 2.48), 1.95 (95% CI: 1.20, 3.19), and 2.77 (95% CI: 1.60, 4.79) (p-trend = 0.0003); this effect was modified by the RNASEL R462Q polymorphism (p interaction = 0.01). Among men with the QQ/RQ genotype, the association between total trans fatty acid intake and prostate cancer was substantially stronger (ORs of higher quartiles equal to 2.93 (95% CI: 1.62, 5.30), 3.13 (95% CI: 1.64, 5.98), and 4.80 (95% CI: 2.29, 10.08), respectively). For men with the RR genotype, total trans fatty acid intake was not associated with disease. This suggests that among Caucasians, positive association between higher trans fatty acid consumption and prostate cancer may be modified by the functional RNASEL variant R462Q.
Key Words: RNASEL • trans fatty acids • prostate cancer
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