脑卒中后的表观遗传年龄和长期癌症风险
Antoni Suárez-Pérez1,2,3, Adrià Macias-Gómez1,2,3, Isabel Fernández-Pérez1,2,3
1Neurovascular Research Group, Hospital del Mar Medical Research Institute, Barcelona, Spain.
Genome medicine
|November 23, 2024
概括
加速表观遗传衰老,通过汉纳姆的外部表观遗传衰老加速 (EEAA) 来衡量,与脑血管事件后 (CVE) 癌症风险增加有关. 这一发现强调了生物衰老加速是中风后癌症发展的关键因素.
科学领域:
- 老年学是一门学科.
- 在瘤学瘤学.
- 神经学 神经学
背景情况:
- 已知脑血管事件 (CVEs) 与癌症风险增加之间存在关联.
- 生物年龄 (B-age) 加速被假设为将CVE与随后的癌症发展联系在一起的潜在机制.
- 这项研究调查了B-age加速作为CVE后癌症发病率的新贡献因素.
研究的目的:
- 检查生物衰老加速在脑血管事件后癌症发展中的作用.
- 确定外部表观遗传衰老加速 (EEAA) 和内部表观遗传衰老加速 (IEAA) 是否与CVE后的癌症发病率有关.
主要方法:
- 对648名潜在中风患者的表观遗传数据进行分析,这些患者以前没有癌症史,并且至少进行了3个月的随访.
- 估计B-age使用DNA甲基化数据从全血样本在中风发作后24小时内,采用多个表观遗传钟.
- 计算EEAA和IEAA,然后评估它们与癌症发病率的独立关联,控制混因素.
主要成果:
- 在648名患者中 (平均随访时间为8.15年),83人 (12.8%) 患上了癌症.
- 考克斯的多变量分析显示,EEAA (Hannum,Zhang,epiTOC) 与CVE后的癌症风险之间存在显著的关联.
- 汉纳姆的EEAA独立预测了癌症风险,经过调整后,加速衰老的发病率每年增加6.0% (HR 1.06 [1.02-1.10],p=0.002).
结论:
- 表观遗传加速衰老,特别是汉纳姆的EEAA,是脑血管事件幸存者观察到的癌症风险增加的一个重要因素.
- 这些发现表明,在CVE后的患者中,癌症风险分层的潜在生物标志物.
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