A functional insertion/deletion polymorphism in the promoter region of the NFKB1 gene increases susceptibility for prostate cancer.

Among men, cancers of the prostate, lung and bronchus, and colon and rectum account for about 50% of all newly diagnosed cancers, and prostate cancer alone accounts for about 25% of incident cases. Nuclear factor-kappaB (NF-kappaB)-activation plays a critical role in prostate cancer by NF-kappaB inhibitor kinase beta pathway-mediated inflammatory-induced tumorigenesis. A functional insertion/deletion polymorphism (-94 insertion/deletion ATTG) in the promoter of the NFKB1 gene, which encodes the p50 subunit of NF-kappaB, was identified recently. A total of 117 prostate cancer patients and 143 control subjects were recruited in this study. The NFKB1 -94 insertion/deletion ATTG genotype was determined using polymerase chain reaction-polyacrylamide gel electrophoresis. The frequency of the ATTG(2) allele in prostate cancer patients was significantly higher than that in the controls (63.7 vs. 54.5%; P=0.035, OR=1.461). Prostate cancer patients with a history of prostatitis have a 2.275 times higher risk for prostate cancer, compared to the control group (P=0.001). The functional NFKB1 promoter polymorphism is associated with increased risk of prostate cancer.