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Interactions of sequence variants in interieukin-1 receptor-associated kinase4 and the Toll-like receptor 6-1-10 gene cluster increase prostate cancer risk
Karolinska institutet, Sweden.ORCID iD: 0000-0003-2046-5641
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2006 (English)In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 15, no 3, p. 480-485Article in journal (Refereed) Published
Abstract [en]

Chronic or recurrent inflammation has been suggested as a causal factor in several human malignancies, including prostate cancer. Genetic predisposition is also a strong risk factor in the development of prostate cancer. In particular, Toll-like receptors (TLR), especially the TLR6-1-10 gene cluster, are involved in prostate cancer development. Interleukin-1 receptor-associated kinases (IRAK) 1 and 4 are critical components in the TLR signaling pathway. In this large case-control study, we tested two hypotheses: (a) sequence variants in IRAK1 and IRAK4 are associated with prostate cancer risk and (b) sequence variants in IRAK1/4 and TLR1-6-10 interacts and confers a stronger risk to prostate cancer. We analyzed 11 single nucleotide polymorphisms (four in IRAK1 and seven in IRAK4) among 1,383 newly diagnosed prostate cancer patients and 780 population controls in Sweden. Although the single-nucleotide polymorphisms in IRAK1 and IRAK4 alone were not significantly associated with prostate cancer risk, one single-nucleotide polymorphism in IRAK4, when combined with the high-risk genotype at TLR6-1-10, conferred a significant excess risk of prostate cancer. In particular, men with the risk genotype at TLR6-1-10 and IRAK4-7987 CG/CC had an odds ratio of 9.68 (P = 0.03) when compared with men who had wildtype genotypes. Our findings suggest synergistic effects between sequence variants in IRAK4 and the TLR 6-1-10 gene cluster. Although this study was based on a priori hypothesis and was designed to address many common issues facing this type of study, our results need confirmation in even larger studies.

Place, publisher, year, edition, pages
Wake Forest Univ, Sch Med, Ctr Human Genom, Winston Salem, NC 27109 USA. Wake Forest Univ, Sch Med, Dept Publ Hlth Sci, Winston Salem, NC 27109 USA. Umea Univ, Dept Radiat Sci, Umea, Sweden. Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden. Univ Hosp Uppsala, Reg Oncol Ctr, Uppsala, Sweden. Orebro Univ Hosp, Dept Urol & Clin Med, Orebro, Sweden. Johns Hopkins Med Inst, Dept Urol, Baltimore, MD USA.: AMER ASSOC CANCER RESEARCH , 2006. Vol. 15, no 3, p. 480-485
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URN: urn:nbn:se:mdh:diva-40721DOI: 10.1158/1055-9965.EPI-05-0645ISI: 000236168200015PubMedID: 16537705OAI: oai:DiVA.org:mdh-40721DiVA, id: diva2:1246150
Available from: 2018-09-06 Created: 2018-09-06 Last updated: 2018-09-06Bibliographically approved

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