Abstract
BackgroundInflammation has been implicated as an etiological factor in several human cancers, including prostate cancer. Allelic variants of the genes involved in inflammatory pathways are logical candidates as genetic determinants of prostate cancer risk. The purpose of this study was to investigate whether single nucleotide polymorphisms of genes that lead to increased levels of pro-inflammatory cytokines and chemokines are associated with an increased prostate cancer risk.MethodsA case-control study design was used to test the association between prostate cancer risk and the polymorphisms TNF-A-308 A/G (rs 1800629), RANTES-403 G/A (rs 2107538), IL1-A-889 C/T (rs 1800587) and MCP-1 2518 G/A (rs 1024611) in 296 patients diagnosed with prostate cancer and in 311 healthy controls from the same area.ResultsDiagnosis of prostate cancer was significantly associated with TNF-A GA + AA genotype (OR, 1.61; 95% CI, 1.09–2.64) and RANTES GA + AA genotype (OR, 1.44; 95% CI, 1.09–2.38). A alleles in TNF-A and RANTES influenced prostate cancer susceptibility and acted independently of each other in these subjects. No epistatic effect was found for the combination of different polymorphisms studied. Finally, no overall association was found between prostate cancer risk and IL1-A or MCP-1 polymorphisms.ConclusionOur results and previously published findings on genes associated with innate immunity support the hypothesis that polymorphisms in proinflammatory genes may be important in prostate cancer development.
Highlights
Inflammation has been implicated as an etiological factor in several human cancers, including prostate cancer
MCP-1 2518 G/A and IL-1 A- 889 T allele genotypes showed no significant differences between prostate cancer and control groups (Table 2), suggesting that these two genotypes may not play a role in susceptibility to prostate cancer
In this case-control study, we investigated the association between polymorphisms in cytokine/chemokine genes (TNF-A -308 G/A, RANTES-403 G/A, IL-1A 889 C/T and MCP-1 2518 G/A) and prostate cancer risk
Summary
Inflammation has been implicated as an etiological factor in several human cancers, including prostate cancer. Allelic variants of the genes involved in inflammatory pathways are logical candidates as genetic determinants of prostate cancer risk. The purpose of this study was to investigate whether single nucleotide polymorphisms of genes that lead to increased levels of proinflammatory cytokines and chemokines are associated with an increased prostate cancer risk. Numerous mediators released in dysregulated chronic inflammation have been found to promote cell growth and invasion, induce mutagenesis and increase angiogenicity [1]. By virtue of these properties, inflammatory mediators favour initiation of malignancy, and if sustained, may promote progression. Pro-inflammatory cytokines (e.g. IL-1 and TNF), can themselves affect cancer risk [1,5,8,19]
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