表观基因组是否有助于癌症发病的风险分层?

NAR Cancer Pub Date : 2021-11-01 eCollection Date: 2021-12-01 DOI:10.1093/narcan/zcab043
Sophie A Lelièvre
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引用次数: 3

摘要

日益增加的癌症负担要求识别和保护高危人群。由于以下原因,表观基因组为风险分层方法的遗传改变提供了不可或缺的补充:癌症发病所需的基因转录是由表观遗传修饰指导的,迄今为止研究的许多危险因素都与表观基因组相关的改变有关。风险水平取决于对环境和饮食影响特别敏感的生命阶段表观基因组的可塑性。DNA调控区活性的改变和染色质压实的改变可能会累积,从而导致癌症风险的增加。此外,组织结构指导着每一种组织和细胞类型的表观基因组的独特组织,这使得表观基因组能够控制特定器官的癌症风险。对风险的表观遗传特征的研究应该有助于确定导致表观基因组无法维持稳态的阈值的连续变化。我们认为这个阈值可能在群体中与给定组织相似,但达到这个阈值的速度将取决于种系遗传和遇到的风险和保护因素的组合,特别是在个体的表观遗传易感性窗口期间。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Can the epigenome contribute to risk stratification for cancer onset?

Can the epigenome contribute to risk stratification for cancer onset?

Can the epigenome contribute to risk stratification for cancer onset?

The increasing burden of cancer requires identifying and protecting individuals at highest risk. The epigenome provides an indispensable complement to genetic alterations for a risk stratification approach for the following reasons: gene transcription necessary for cancer onset is directed by epigenetic modifications and many risk factors studied so far have been associated with alterations related to the epigenome. The risk level depends on the plasticity of the epigenome during phases of life particularly sensitive to environmental and dietary impacts. Modifications in the activity of DNA regulatory regions and altered chromatin compaction may accumulate, hence leading to the increase of cancer risk. Moreover, tissue architecture directs the unique organization of the epigenome for each tissue and cell type, which allows the epigenome to control cancer risk in specific organs. Investigations of epigenetic signatures of risk should help identify a continuum of alterations leading to a threshold beyond which the epigenome cannot maintain homeostasis. We propose that this threshold may be similar in the population for a given tissue, but the pace to reach this threshold will depend on the combination of germline inheritance and the risk and protective factors encountered, particularly during windows of epigenetic susceptibility, by individuals.

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