Genetic variability in inflammation pathways and prostate cancer risk

Jielin Sun, Aubrey Turner, Jianfeng Xu, Henrik Grönberg, William Isaacs

Research output: Contribution to journalReview article

Abstract

Genetic susceptibility to prostate cancer has been consistently observed by a large number of studies. Recently, several pieces of evidence obtained from epidemiological and pathological studies support that chronic inflammation in prostate tissues may play a role in prostate cancer development. Multiple genes that play critical roles in inflammatory pathways have been associated with prostate cancer risk. In this article we review the key genetic findings of the associated genes. This includes 2 genes identified through family studies, ribonuclease L (RNASEL) and macrophage scavenger receptor 1 (MSR1), as well as a number of genes suggested by case-control studies, such as macrophage inhibitory cytokine-1 (MIC-1), interleukins (IL-8, IL-10), vascular endothelial growth factor (VEGF), intercellular adhesion molecule (ICAM), and Toll-like receptors (TLR-4, TLR-1-6-10 gene cluster). Overall, recent studies seem to suggest multiple genes work together to increase prostate risk, and this is consistent with the reality that inflammation is a very complex process. Thus, future studies are expected to place an emphasis on the study of gene-gene interactions. Advances in high throughput genotyping, data mining, and algorithm development are needed in order to produce interpretable results.

Original languageEnglish (US)
Pages (from-to)250-259
Number of pages10
JournalUrologic Oncology: Seminars and Original Investigations
Volume25
Issue number3
DOIs
StatePublished - May 1 2007

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Keywords

  • Genetic variability
  • Inflammation
  • MSR1
  • Mutation
  • Prostate cancer
  • RNASEL
  • SNP
  • TLR

ASJC Scopus subject areas

  • Oncology
  • Urology

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