%0 Journal Article
%T Genetic polymorphisms of RANTES, IL1-A, MCP-1 and TNF-A genes in patients with prostate cancer
%A Pablo S¨˘enz-L¨®pez
%A Rafael Carretero
%A Jos¨¦ C¨®zar
%A Jos¨¦ Romero
%A Julia Canton
%A Jos¨¦ Vilchez
%A Miguel Tallada
%A Federico Garrido
%A Francisco Ruiz-Cabello
%J BMC Cancer
%D 2008
%I BioMed Central
%R 10.1186/1471-2407-8-382
%X A 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.Diagnosis of prostate cancer was significantly associated with TNF-A GA + AA genotype (OR, 1.61; 95% CI, 1.09¨C2.64) and RANTES GA + AA genotype (OR, 1.44; 95% CI, 1.09¨C2.38). 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.Our 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.Chronic or recurrent inflammation is known to play a causative role in the promotion and progression of many human tumours, including cancers of the liver, oesophagus, stomach, large intestine and urinary bladder [1-3]. Chronic inflammation has also been implicated in the aetiology of prostate cancer [4-7]. Prostate cancer risk has been associated with sexually transmitted infections and prostatitis in some epidemiologic studies [8,9], and its relationship with genetic polymorphisms in inflammatory cytokines has been explored in various case-control studies [10-13]. Chronic inflammation, alongside the intrinsic properties of pre-malignant cells and other determinants, may therefore be one of the driving forces of malignant transformation. Thus, 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 favo
%U http://www.biomedcentral.com/1471-2407/8/382