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本文引用的文献

1
Gene environment interactions with a novel variable Monoamine Oxidase A transcriptional enhancer are associated with antisocial personality disorder.基因-环境相互作用与新型单胺氧化酶 A 转录增强子有关,与反社会人格障碍有关。
Biol Psychol. 2011 Jul;87(3):366-71. doi: 10.1016/j.biopsycho.2011.04.007. Epub 2011 May 7.
2
Behavioral genetics in antisocial spectrum disorders and psychopathy: a review of the recent literature.反社会谱系障碍和精神病态的行为遗传学:对近期文献的综述。
Behav Sci Law. 2010 Mar-Apr;28(2):148-73. doi: 10.1002/bsl.923.
3
Serotonin activates MAP kinase and PI3K/Akt signaling pathways in prostate cancer cell lines.血清素激活前列腺癌细胞系中的 MAP 激酶和 PI3K/Akt 信号通路。
Urol Oncol. 2011 Jul-Aug;29(4):436-45. doi: 10.1016/j.urolonc.2009.09.013. Epub 2009 Nov 19.
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Statin use and risk of prostate cancer: results from a population-based epidemiologic study.他汀类药物的使用与前列腺癌风险:一项基于人群的流行病学研究结果
Am J Epidemiol. 2008 Aug 1;168(3):250-60. doi: 10.1093/aje/kwn141. Epub 2008 Jun 12.
5
MAOA methylation is associated with nicotine and alcohol dependence in women.单胺氧化酶A(MAOA)甲基化与女性的尼古丁和酒精依赖有关。
Am J Med Genet B Neuropsychiatr Genet. 2008 Jul 5;147B(5):565-70. doi: 10.1002/ajmg.b.30778.
6
Inhibition of monoamine oxidase A promotes secretory differentiation in basal prostatic epithelial cells.单胺氧化酶A的抑制促进前列腺基底上皮细胞的分泌分化。
Differentiation. 2008 Sep;76(7):820-30. doi: 10.1111/j.1432-0436.2007.00263.x. Epub 2008 Jan 31.
7
A molecular correlate to the Gleason grading system for prostate adenocarcinoma.前列腺腺癌Gleason分级系统的分子关联因素。
Proc Natl Acad Sci U S A. 2006 Jul 18;103(29):10991-6. doi: 10.1073/pnas.0603678103. Epub 2006 Jul 7.
8
Type A monoamine oxidase is the target of an endogenous dopaminergic neurotoxin, N-methyl(R)salsolinol, leading to apoptosis in SH-SY5Y cells.A型单胺氧化酶是内源性多巴胺能神经毒素N-甲基(R)-四氢哈尔满的作用靶点,可导致SH-SY5Y细胞凋亡。
J Neurochem. 2006 Jan;96(2):541-9. doi: 10.1111/j.1471-4159.2005.03573.x. Epub 2005 Dec 8.
9
Redox redux: revisiting PTPs and the control of cell signaling.氧化还原再探:重新审视蛋白酪氨酸磷酸酶与细胞信号传导的控制
Cell. 2005 Jun 3;121(5):667-70. doi: 10.1016/j.cell.2005.05.016.
10
Striatal damage and oxidative stress induced by the mitochondrial toxin malonate are reduced in clorgyline-treated rats and MAO-A deficient mice.在氯吉兰处理的大鼠和单胺氧化酶A缺乏的小鼠中,线粒体毒素丙二酸酯诱导的纹状体损伤和氧化应激有所减轻。
Neurochem Res. 2004 Apr;29(4):741-6. doi: 10.1023/b:nere.0000018845.82808.45.

单胺氧化酶 A 基因启动子重复与前列腺癌风险。

The monoamine oxidase A gene promoter repeat and prostate cancer risk.

机构信息

Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109-1024, USA.

出版信息

Prostate. 2012 Nov;72(15):1622-7. doi: 10.1002/pros.22515. Epub 2012 Apr 2.

DOI:10.1002/pros.22515
PMID:22473857
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3532925/
Abstract

BACKGROUND

Amine catabolism by monoamine oxidase A (MAOA) contributes to oxidative stress, which plays a role in prostate cancer (PCa) development and progression. An upstream variable-number tandem repeat (uVNTR) in the MAOA promoter influences gene expression and activity, and may thereby affect PCa susceptibility.

METHODS

Caucasian (n = 2,572) men from two population-based case-control studies of PCa were genotyped for the MAOA-VNTR. Logistic regression was used to assess PCa risk in relation to genotype.

RESULTS

Common alleles of the MAOA-VNTR were not associated with the relative risk of PCa, nor did the relationship differ by clinical features of the disease. The rare 5-copy variant (frequency: 0.5% in cases; 1.8% in controls), however, was associated with a reduced PCa risk (odds ratio, OR = 0.30, 95% CI 0.13-0.71).

CONCLUSIONS

A rare polymorphism of the MAOA promoter previously shown to confer low expression was associated with a reduced risk of developing PCa. This novel finding awaits confirmation in other study populations.

摘要

背景

单胺氧化酶 A(MAOA)的胺类代谢产物会导致氧化应激,这在前列腺癌(PCa)的发生和发展中起着一定的作用。MAOA 启动子中的一个上游可变数串联重复(uVNTR)会影响基因表达和活性,从而可能会影响 PCa 的易感性。

方法

对来自两项基于人群的 PCa 病例对照研究的 2572 名白种人男性进行 MAOA-VNTR 基因分型。采用 logistic 回归分析评估基因型与 PCa 风险之间的关系。

结果

MAOA-VNTR 的常见等位基因与 PCa 的相对风险无关,与疾病的临床特征也没有关系。然而,罕见的 5 拷贝变异体(频率:病例组为 0.5%;对照组为 1.8%)与 PCa 风险降低相关(比值比,OR=0.30,95%CI 0.13-0.71)。

结论

先前研究表明,MAOA 启动子的罕见多态性与低表达相关,与 PCa 发病风险降低有关。这一新颖的发现需要在其他研究人群中得到证实。