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.
Cancers (Basel). 2010 Jun 8;2(2):1198-220. doi: 10.3390/cancers2021198.
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.
前列腺癌是西方社会男性中最常见的癌症，随着全球人口老龄化，其发病率预计将会上升。然而，前列腺癌的病因尚不清楚，而目前的诊断工具可能具有侵入性（直肠指检或活检）和/或缺乏对该疾病的特异性（前列腺特异性抗原（PSA）检测）。大量的组织学、流行病学和分子遗传学证据表明，炎症在前列腺癌的发病机制中很重要。在这篇综述中，我们总结了影响前列腺癌易感性的炎症遗传标记物的现状。重点将放在调节辅助性 T 细胞和趋化因子平衡的炎症细胞因子上，以及作为宿主固有免疫系统关键因子的 Toll 样受体上。尽管由于缺乏复制，目前表明前列腺癌具有遗传基础的关联研究受到限制，但更大、更具种族和临床定义的研究人群可能有助于阐明炎症基因变异对前列腺癌风险的真正贡献。
