Journal Article

Interactions of cytokine gene polymorphisms in prostate cancer risk

Jovanny Zabaleta, Hui-Yi Lin, Rosa A. Sierra, M.Craig Hall, Peter E. Clark, Oliver A. Sartor, Jennifer J. Hu and Augusto C. Ochoa

in Carcinogenesis

Volume 29, issue 3, pages 573-578
Published in print March 2008 | ISSN: 0143-3334
Published online January 2008 | e-ISSN: 1460-2180 | DOI:
Interactions of cytokine gene polymorphisms in prostate cancer risk

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Prostate cancer (CaP) is the second leading cause of cancer death in American men. Chronic inflammation has been one of several factors associated with the development of CaP. Single-nucleotide polymorphisms (SNPs) in cytokine genes have been associated with increased inflammation, increased cytokine production and possibly increased CaP risk. However, the effects of cytokine SNPs on CaP susceptibility have not been consistent. Using the genomic DNA collected in a CaP case–control study (557 cases and 547 controls), we pilot tested the interactions of nine functionally characterized SNPs of three cytokine genes in CaP risk using the multivariate adaptive regression splines (MARS)–logit models. African-Americans with the IL10−819TT genotype had a lower CaP risk [odds ratio (OR) = 0.27, 95% confidence interval (CI) = 0.07–1.01], but subjects with the genotype combination of IL1B−511CT/TT and IL10−592CC had a higher CaP risk (OR = 2.56, 95% CI = 1.09–6.02). In Caucasians, higher CaP risk was associated with the IL10−1082AG/GG genotype (OR = 3.62, 95% CI = 1.42–9.28), the genotype combination of IL10−1082AA plus IL1B−31TT/TC (OR = 2.92, 95% CI = 1.13–7.55) and the genotype combination of TNF−238GG plus IL10−592AA (OR = 2.14, 95% CI = 1.05–4.38). Our results highlight the importance of cytokine SNPs and their interactions in CaP risk.

Journal Article.  4059 words.  Illustrated.

Subjects: Clinical Cytogenetics and Molecular Genetics

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