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Article

Interactions of sequence variants in interleukin-1 receptor-associated kinase4 and the toll-like receptor 6-1-10 gene cluster increase prostate cancer risk.

Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology - 1 Mar 2006

Sun Jielin, Wiklund Fredrik, Hsu Fang-Chi, Bälter Katarina, Zheng S Lilly, Johansson Jan-Erik, Chang Baoli, Liu Wennuan, Li Tao, Turner Aubrey R, Li Liwu, Li Ge, Adami Hans-Olov, Isaacs William B, Xu Jianfeng, Grönberg Henrik

Abstract excerpt

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 clus...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Source

Identifiers

PMID: 16537705
DOI: 10.1158/1055-9965.EPI-05-0645

Genes

IRAK4
IRAK1
TLR6
TLR1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 2 Sept 2026. Prepared record publication-16537705-2026-09-02.2. Manifest publication-graph-cohort-2026-09-02.2.

Source receipt: PubMed via Helena Literature Corpus, retrieved 2 Sept 2026.

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Interactions of sequence variants in interleukin-1 receptor-associated kinase4 and the toll-like receptor 6-1-10 gene cluster increase prostate cancer risk.PMID 16537705Read ↗

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