Inflammatory Genetic Markers of Prostate Cancer Risk

Cancers

Elizabeth A. Tindall¹  Vanessa M. Hayes¹ 

[1] Cancer Genetics Group, Children’s Cancer Institute Australia for Medical Research, Lowy Cancer Research Centre, University of New South Wales, PO Box 81, Randwick, NSW 2031, Australia; E-Mails:

关键词: prostate cancer;    inflammation;    Toll like receptor (TLR);    cytokine;    chemokine;    gene variant;    inherited susceptibility;   

DOI  :  10.3390/cancers2021198

来源: mdpi

【 摘 要 】

Prostate cancer is the most common cancer in Western society males, with incidence rates predicted to rise with global aging. Etiology of prostate cancer is however poorly understood, while current diagnostic tools can be invasive (digital rectal exam or biopsy) and/or lack specificity for the disease (prostate-specific antigen (PSA) testing). Substantial histological, epidemiological and molecular genetic evidence indicates that inflammation is important in prostate cancer pathogenesis. In this review, we summarize the current status of inflammatory genetic markers influencing susceptibility to prostate cancer. The focus will be on inflammatory cytokines regulating T-helper cell and chemokine homeostasis, together with the Toll-like receptors as key players in the host innate immune system. Although association studies indicating a genetic basis for prostate cancer are presently limited mainly due to lack of replication, larger and more ethnically and clinically defined study populations may help elucidate the true contribution of inflammatory gene variants to prostate cancer risk.

【 授权许可】

CC BY   
© 2010 by the authors; licensee MDPI, Basel, Switzerland.