The DNA methylation signature of smoking: an archetype for the identification of biomarkers for behavioral illness.
The DNA methylation signature of smoking: an archetype for the identification of biomarkers for behavioral illness.
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吸烟的 DNA 甲基化特征：识别行为疾病生物标志物的原型。
DOI：
10.1007/978-1-4939-0653-6_6
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发表时间：
2014
期刊：
影响因子：
--
通讯作者：
Brody,GeneH
中科院分区：
文献类型：
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作者：
Philibert,RobertA;Beach,SRH;Brody,GeneH
吸烟可能是美国和世界上最重要的公共卫生挑战。在一系列迅速出现的研究中，我们和其他人已经证明吸烟与外周血细胞DNA甲基化特征的变化有关。与这类物质使用相关的变化是剂量和时间依赖性的。DNA甲基化的这些变化还伴随着基因转录和蛋白质表达的变化，其模式进一步表明对其他形式的复杂疾病的易感性增加。过去，我们将这些知识转化为可操作信息的努力因缺乏系统评估这些变化的方法而受阻。DNA甲基化评估技术的快速发展改变了这种动态，并提出了开发基于甲基化的临床工具以帮助确定吸烟状态或治疗有效性的可能性。在本章中，我们回顾了这一领域的最新进展，并讨论了这些进展如何使我们了解通过哪些方法来预防吸烟和摆脱洞察优化策略，通过这些策略来识别其他行为疾病的生物标志物，这些疾病具有类似的环境和基因-环境相互作用效应。
Smoking is perhaps the foremost public health challenge in the USA and in the world. In a series of rapidly emerging studies, we and others have demonstrated that cigarette smoking is associated with changes in the DNA methylation signature of peripheral blood cells. The changes associated with this type of substance use are both dose and time dependent. These changes in DNA methylation are also accompanied by changes in gene transcription and protein expression whose patterns are furthermore indicative of increased vulnerability to other forms of complex illness. In the past, our efforts to translate this knowledge into actionable information have been stymied by a lack of methods through which to systematically assess these changes. The rapid advance of DNA methylation assessment technologies changes that dynamic and presents the possibility that methylation-based clinical tools to aid the ascertainment of smoking status or effectiveness of treatment can be developed. In this chapter, we review the latest advances in this field and discuss how these advances allow us insight as to methods through which to prevent smoking and shed insight into optimizing strategies through which to identify biomarkers for other behavioral illnesses which share similar contributions from environmental and gene–environmental interaction effects.