Display Settings:


Send to:

Choose Destination
See comment in PubMed Commons below
Cancer Causes Control. 2010 Sep;21(9):1437-44. doi: 10.1007/s10552-010-9571-0. Epub 2010 Apr 30.

Polymorphisms in inflammatory genes, plasma antioxidants, and prostate cancer risk.

Author information

  • 1Department of Public Health, Indiana University School of Medicine, Indianapolis, IN 46202, USA. jz21@iupui.edu



Presence of xenotropic murine leukemia virus-related virus and chronic inflammation in prostate tumor suggests that inflammation plays a role in prostate cancer etiology. This study investigated whether variants in inflammatory genes act alone or interact with plasma antioxidants to influence prostate cancer risk in a population-based case-control study in Central Arkansas.


Cases (n = 193) were men, aged 40-80, diagnosed with prostate cancer in three major hospitals in 1998-2003, and controls (n = 197) were matched to cases by age, race, and county of residence.


After adjustment for confounders, polymorphisms in COX-2 (rs689466) and IL-8 (rs4073) were not significantly associated with prostate cancer risk. However, apparent interactions were observed between these genetic variants and plasma antioxidants on the risk of this malignancy. The protective effect of the mutant allele of the COX-2 polymorphism was more pronounced among subjects with high plasma levels of beta-cryptoxanthin, lycopene, beta-carotene, or selenium (>or=median) [e.g., OR (95% CI): 0.37 (0.15, 0.86) (AG/GG vs. AA) for beta-cryptoxanthin]. Conversely, the promoting effect of the variant allele of the IL-8 polymorphism was more remarkable in subjects with low plasma levels of Lutein/zeaxanthin, beta-cryptoxanthin, and beta-carotene (<median) [e.g., OR (95% CI): 2.44 (1.08, 5.75) (AT/TT vs. AA) for beta-carotene].


We found that sequence variants in inflammatory genes interact with plasma antioxidants to modulate prostate cancer risk.

[PubMed - indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Springer Icon for PubMed Central
    Loading ...
    Write to the Help Desk