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在MRONJ中综合表观基因组和向蛋白质分析:将DNA甲基化与骨生物标志物的相关性

Raed Awadh Alshammari^1,2, Marwa Tantawy¹, Danxin Wang¹

¹Department of Pharmacotherapy and Translational Research and Center for Pharmacogenomics and Precision Medicine, College of Pharmacy, University of Florida, Gainesville, FL 32610, USA.

International journal of molecular sciences

|November 27, 2025

概括

癌症患者的表观遗传变化可能预测与药物相关的下巴骨硬化 (MRONJ). 这项研究确定了与接受骨修饰剂治疗的患者中与MRONJ发育相关的特定DNA甲基化位点.

科学领域:

基因组学就是基因组学.
在瘤学瘤学.
药理学药理学是指药理学的学科.

背景情况:

与药物相关的下巴骨硬化 (MRONJ) 是抗吸收疗法 (如双酸盐 (BPs) 和代诺苏马布 (DMB)) 的严重并发症.
了解MRONJ背后的表观遗传机制对于接受这些治疗的癌症患者的风险评估和预防至关重要.

研究的目的:

在接受BP或BP+DMB治疗的癌症患者中,研究与MRONJ相关的DNA甲基化差异.
为了确定MRONJ风险的潜在表观遗传生物标志物.

主要方法:

在24名癌症患者中使用Infinium®甲基化EPIC v2.0阵列进行了全表观基因组关联研究 (EWAS).
进行了病例控制分析,将MRONJ患者与对照进行比较,按治疗分层 (仅BP与BP/DMB).
量化了八种血骨生物标志物,并将它们与已识别的甲基化位点相关联.

主要成果:

确定了10个差异甲基化位置 (DMP) 和4个差异甲基化区域 (DMR) 的暗示意义 (p < 1 × 10−5).
改变甲基化的关键基因包括NOP56 (低甲基化,与骨素相关),TNXB (高甲基化),PDE8A (低甲基化) 和TRIM15.
基因TNXB,TRIM15和PDE8A参与了原I调节;NOP56参与了核糖体生物发生.

结论:

初步发现表明,NOP56,TNXB,PDE8A和TRIM15中的特定表观遗传变化可能有助于MRONJ的发展.
这些表观遗传变化可能会影响原I合成和核糖体生物发生,需要进一步研究.
由于样本规模较小,需要进行更大规模的验证研究.

关键词:

通过DNA甲基化.骨蛋白质生物标志物生物标志物骨头改造骨头改造骨头改造表观遗传学是指表观遗传学.全表观基因组关联研究 (EWAS)与药物相关的下巴骨硬化 (MRONJ)

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