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在 silico 和 in vitro 方法表明,在接受Entrectinib 治疗的儿童中,骨质细胞生成诱导潜在骨折

Sabrina Ehnert¹, Andreas K Nüssler², Kevin A Schulz²

¹Department of Trauma and Reconstructive Surgery, Siegfried Weller Research Institute, BG Unfallklinik Tübingen, University of Tübingen, Schnarrenbergstr. 95, 72076, Tübingen, Germany. Sabrina.Ehnert@med.uni-tuebingen.de.

Archives of toxicology

|June 25, 2025

概括

恩特雷克提尼布治疗可能会通过抑制骨形成和刺激骨再吸收,导致儿童骨折. 维生素D可能提供一种保护策略,防止这些影响骨发育.

科学领域:

在瘤学瘤学.
药理学药理学是指药理学的学科.
儿科儿科儿科
生物化学生物化学

背景情况:

恩特雷克提尼布是一种TRK和ROS1抑制剂,用于癌症治疗.
骨折是Entrectinib观察到的一种副作用,特别是在儿科患者中.
恩特雷克提尼布诱导的骨折背后的确切机制尚不清楚.

研究的目的:

调查儿科患者因恩特雷克提尼布相关骨折的潜在机制.
探索因恩特雷克提尼布诱导的骨毒性潜在的缓解策略.

主要方法:

利用基于人工智能 (AI) 的方法来生成假设.
使用人类骨细胞培养物 (骨质母细胞和骨质母细胞) 进行了体外研究.
进行了3D骨质母细胞-骨质母细胞共同培养和途径分析.

主要成果:

人工智能分析表明,恩特雷克提尼布抑制TRK和JAK2,影响骨细胞.
恩特雷克提尼布降低了骨质母细胞活性和矿化,同时增加了骨质母细胞骨的再吸收.
观察到骨硬度降低,特别是在缺乏17β-雌二醇的青少年骨模型中.
鉴定出抑制骨生长调节剂TGF-β和BMP.

结论:

恩特雷克提尼布对骨细胞的影响表明,有针对性机制导致儿童骨折.
在实验室中,维生素D部分恢复了骨质细胞功能,并抑制了骨质细胞的活性.
需要进一步的临床试验数据来确认这些发现并验证缓解策略.

关键词:

骨共同培养是一种骨共同培养.在Entrectinib上使用.在模型建模.骨质细胞生成 (Osteoclastogenesis) 是一个过程.儿科骨折儿科骨折是指儿童的骨折.

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