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[Cancer Research 62, 3369-3372, June 15, 2002]
© 2002 American Association for Cancer Research

Advances in Brief

Influence of Cytokine Gene Polymorphisms on the Development of Prostate Cancer1

Sarah L. McCarron, Stephen Edwards, Philip R. Evans, Roz Gibbs, David P. Dearnaley, Anna Dowe, Christine Southgate The Cancer Research Campaign/British Prostate Group United Kingdom Familial Prostate Cancer Study Collaborators2, Douglas F. Easton, Rosalind A. Eeles and W. Martin Howell3

Department of Histocompatibility and Immunogenetics, Southampton University Hospitals NHS Trust, Southampton SO16 6YD [S. L. M., P. R. E., W. M. H.]; Institute of Cancer Research, Royal Marsden Hospital NHS Trust, Sutton, Surrey SM2 5PT [S. E., D. P. D., A. D., C. S., R. A. E.]; University of Portsmouth, Portsmouth PO1 2RY [R. G.]; and CRC Genetic Epidemiology Unit, Strangeways Laboratories, Cambridge CB1 4RN [D. F. E.], United Kingdom

Polymorphisms in the promoter regions of cytokine genes may influence prostate cancer (PC) development via regulation of the antitumor immune response and/or pathways of tumor angiogenesis. PC patients (247) and 263 controls were genotyped for interleukin (IL)-1ß-511, IL-8-251, IL-10-1082, tumor necrosis factor-{alpha}-308, and vascular endothelial growth factor (VEGF)-1154 single nucleotide polymorphisms. Patient control comparisons revealed that IL-8 TT and VEGF AA genotypes were decreased in patients compared with controls [23.9 versus 32.3%; P = 0.04, odds ratio (OR) = 0.66, 95% confidence interval (CI) 0.44–0.99 and 6.3 versus 12.9%; P = 0.01, OR = 0.45, 95% CI 0.24–0.86, respectively], whereas the IL-10 AA genotype was significantly increased in patients compared with controls (31.6 versus 20.6%; P = 0.01, OR = 1.78, 95% CI 1.14–2.77). Stratification according to prognostic indicators showed association between IL-8 genotype and log prostate-specific antigen level (P = 0.05). These results suggest that single nucleotide polymorphisms associated with differential production of IL-8, IL-10, and VEGF are risk factors for PC, possibly acting via their influence on angiogenesis.




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