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Inflammatory Genetic Markers of Prostate Cancer Risk

机译:前列腺癌风险的炎性遗传标记

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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.
机译:前列腺癌是西方社会男性中最常见的癌症,其发病率预计会随着全球老龄化而上升。然而,对前列腺癌的病因学知之甚少,而当前的诊断工具可能是侵入性的(直肠指检或活检)和/或缺乏对疾病的特异性(前列腺特异性抗原(PSA)测试)。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理中很重要。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志物的现状。重点将放在调节T辅助细胞和趋化因子稳态的炎性细胞因子,以及Toll样受体作为宿主先天免疫系统的关键角色。尽管目前表明前列腺癌遗传基础的关联研究主要是由于缺乏复制而受到限制,但更大,更多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。

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