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雄激素信号通路多态性与前列腺癌易感性。

Polymorphisms in androgen signaling pathway predisposing to prostate cancer.

机构信息

Institute of Biomedical Technology, University of Tampere, and Centre for Laboratory Medicine, Tampere University Hospital, Biokatu 8, 33520 Tampere, Finland.

出版信息

Mol Cell Endocrinol. 2012 Sep 5;360(1-2):25-37. doi: 10.1016/j.mce.2011.07.007. Epub 2011 Jul 18.

DOI:10.1016/j.mce.2011.07.007
PMID:21782882
Abstract

Prostate cancer is the most frequent male malignancy diagnosed in western countries and androgens are known to mediate key physiological processes in prostate tissue. Since endogenous androgens have long been considered to be risk factors for prostate cancer, genes involved in androgen biosynthesis and metabolism have been extensively studied. In this review, association of androgen pathway genes, their polymorphic sites and risk of prostate cancer in different ethnic backgrounds is addressed together with their use to predict susceptibility and clinical outcomes of prostate cancer patients. The effect of the polymorphisms seems vary in different patients, populations and ethnic backgrounds. To date it is evident that the association between androgen pathway gene polymorphisms and prostate cancer risk is complex and many of the results are characterized by irreproducibility, which can be attributed to a variety of biological, statistical and technical reasons. In the future, with increasing knowledge, developing technologies and new genomic biomarkers it likely becomes possible to better estimate the risk of prostate cancer, and distinguish indolent disease from aggressive based on molecular profiling, and the analysis of gene-gene and gene-environment interactions.

摘要

前列腺癌是西方国家最常见的男性恶性肿瘤,雄激素被认为是前列腺组织中关键生理过程的介质。由于内源性雄激素一直被认为是前列腺癌的危险因素,因此雄激素生物合成和代谢相关的基因已被广泛研究。在这篇综述中,我们探讨了雄激素通路基因及其多态性位点与不同种族背景下前列腺癌风险的相关性,以及它们在预测前列腺癌患者易感性和临床结局中的应用。多态性的影响似乎因不同的患者、人群和种族背景而异。迄今为止,很明显,雄激素通路基因多态性与前列腺癌风险之间的关联是复杂的,许多结果的特征是不可复制性,这可能归因于多种生物学、统计学和技术原因。未来,随着知识的不断增加、技术的发展和新的基因组生物标志物的出现,我们很可能能够更好地估计前列腺癌的风险,并根据分子谱分析以及基因-基因和基因-环境相互作用的分析,将惰性疾病与侵袭性疾病区分开来。

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1
Polymorphisms in androgen signaling pathway predisposing to prostate cancer.雄激素信号通路多态性与前列腺癌易感性。
Mol Cell Endocrinol. 2012 Sep 5;360(1-2):25-37. doi: 10.1016/j.mce.2011.07.007. Epub 2011 Jul 18.
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Polymorphisms in genes involved in androgen pathways as risk factors for prostate cancer.雄激素途径相关基因多态性作为前列腺癌的危险因素
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The epidemiology of sex steroid hormones and their signaling and metabolic pathways in the etiology of prostate cancer.性类固醇激素及其信号传导和代谢途径在前列腺癌病因学中的流行病学
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[Case-control study of the genes of receptors of the androgens of vitamin-D and of 5-alphareductase in a population of Afro-Caribbean population with prostate cancer].[针对患有前列腺癌的非洲加勒比人群中维生素D雄激素受体基因和5α还原酶基因的病例对照研究]
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Identification of Germline Genetic Variants that Increase Prostate Cancer Risk and Influence Development of Aggressive Disease.鉴定增加前列腺癌风险并影响侵袭性疾病发展的生殖系基因变异。
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2
Genetic Association between Gene Polymorphisms and Risk of Prostate Cancer: A Meta-Analysis.基因多态性与前列腺癌风险之间的遗传关联:一项荟萃分析。
Front Physiol. 2017 Dec 1;8:975. doi: 10.3389/fphys.2017.00975. eCollection 2017.
3
Circulating and intraprostatic sex steroid hormonal profiles in relation to male pattern baldness and chest hair density among men diagnosed with localized prostate cancers.
经诊断患有局限性前列腺癌的男性体内循环和前列腺内性类固醇激素水平与男性型秃发及胸毛密度的关系
Prostate. 2017 Dec;77(16):1573-1582. doi: 10.1002/pros.23433. Epub 2017 Oct 2.
4
Androgen receptor gene polymorphisms and risk of prostate cancer: a meta-analysis.雄激素受体基因多态性与前列腺癌风险:荟萃分析。
Sci Rep. 2017 Jan 16;7:40554. doi: 10.1038/srep40554.
5
Association of androgen metabolism gene polymorphisms with prostate cancer risk and androgen concentrations: Results from the Prostate Cancer Prevention Trial.雄激素代谢基因多态性与前列腺癌风险及雄激素浓度的关联:前列腺癌预防试验的结果
Cancer. 2016 Aug 1;122(15):2332-40. doi: 10.1002/cncr.30071. Epub 2016 May 10.
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Genetic polymorphisms in the androgen metabolism pathway and risk of prostate cancer in low incidence Malaysian ethnic groups.雄激素代谢途径中的基因多态性与马来西亚低发病率族群的前列腺癌风险
Int J Clin Exp Med. 2015 Oct 15;8(10):19232-40. eCollection 2015.
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Acta Pharmacol Sin. 2015 Jan;36(1):3-23. doi: 10.1038/aps.2014.18. Epub 2014 Jun 9.
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