The interaction of four genes in the inflammation pathway significantly predicts prostate cancer risk.

doi:10.1158/1055-9965.EPI-05-0356

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Community

Back to search

Article

The interaction of four genes in the inflammation pathway significantly predicts 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 Nov 2005

Xu Jianfeng, Lowey James, Wiklund Fredrik, Sun Jielin, Lindmark Fredrik, Hsu Fang-Chi, Dimitrov Latchezar, Chang Baoli, Turner Aubrey R, Liu Wennan, Adami Hans-Olov, Suh Edward, Moore Jason H, Zheng S Lilly, Isaacs William B, Trent Jeffrey M, Grönberg Henrik

Abstract excerpt

It is widely hypothesized that the interactions of multiple genes influence individual risk to prostate cancer. However, current efforts at identifying prostate cancer risk genes primarily rely on single-gene approaches. In an attempt to fill this gap, we carried out a study to explore the joint effect of multiple genes in the inflammation pathway on prostate cancer risk. We studied 20 genes in the Toll-like...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Case-Control Studies

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Haplotypes

Share to Inflammation

Share to Prognosis

Share to Prostatic Neoplasms

Share to Registries

Share to Signal Transduction

Share to Toll-Like Receptors

Source

Open in PubMed

Identifiers

PMID: 16284379
DOI: 10.1158/1055-9965.EPI-05-0356

Genes

CAPS
TIRAP
TLR5

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

The interaction of four genes in the inflammation pathway significantly predicts prostate cancer risk.PMID 16284379Read ↗

A comprehensive association study for genes in inflammation pathway provides support for their roles in prostate cancer risk in the CAPS study.Semantic proximity Read ↗

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

Sequence variants in Toll-like receptor gene cluster (TLR6-TLR1-TLR10) and prostate cancer risk.Semantic proximity Read ↗

A Multigene-Panel Study Identifies Single Nucleotide Polymorphisms Associated with Prostate Cancer Risk.Semantic proximity Read ↗

Genetic variation in the toll-like receptor gene cluster (TLR10-TLR1-TLR6) and prostate cancer risk.Semantic proximity Read ↗

Sequence variants in the TLR4 and TLR6-1-10 genes and prostate cancer risk. Results based on pooled analysis from three independent studies.Semantic proximity Read ↗

Interactions of cytokine gene polymorphisms in prostate cancer risk.Semantic proximity Read ↗

Sequence variants of toll-like receptor 4 are associated with prostate cancer risk: results from the CAncer Prostate in Sweden Study.Semantic proximity Read ↗

Association between Toll-like receptor gene cluster (TLR6, TLR1, and TLR10) and prostate cancer.Semantic proximity Read ↗

A multigenic approach to evaluating prostate cancer risk in a systematic replication study.Semantic proximity Read ↗

Toll-like receptor 4 genetic variation and advanced prostate cancer risk.Semantic proximity Read ↗

Genetic variability in inflammation pathways and prostate cancer risk.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.