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Carcinogenesis Advance Access originally published online on January 18, 2007
Carcinogenesis 2007 28(6):1232-1236; doi:10.1093/carcin/bgm002
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© The Author 2007. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

trans-Fatty acid intake and increased risk of advanced prostate cancer: modification by RNASEL R462Q variant

Xin Liu1,4,*, Fredrick R. Schumacher2, Sarah J. Plummer3, Eric Jorgenson1, Graham Casey3 and John S. Witte1,*

1 Department of Epidemiology and Biostatistics and Institute for Human Genetics, University of California, San Francisco, CA 94143-0794, USA
2 Channing Laboratory, Brigham and Women’s Hospital and Department of Epidemiology, Harvard School of Public Health, Boston, MA 02115, USA
3 Department of Cancer Biology, Lerner Research Institute, The Cleveland Clinic, Cleveland, OH 44195, USA
4 Present address: Mary Ann and 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, USA

* To whom correspondence should be addressed. Tel: +1 415 502 6882; Fax: +1 415 476 1356;

Email: wittej{at}humgen.ucsf.edu

Correspondence may also be addressed to Xin Liu. Tel: +1 312 573 7751; Fax: +1 312 573 7825;

Email: xnliu{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 = 1012) 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 with the lowest quartile of total trans-fatty acid consumption, the higher quartiles gave odds ratios (ORs) equal to 1.58 [95% confidence interval (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 (Pinteraction = 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.

Abbreviations: CI, confidence interval; FFQ, food frequency questionnaire; OR, odds ratio

Received September 18, 2006; revised January 5, 2007; accepted January 5, 2007.


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