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解决FGFR3驱动的膀癌,通过一个有前途的协同作用的FGFR/HDAC向性疗法

Zechen Wang¹, Viswanathan Muthusamy², Daniel P Petrylak³

¹Department of Pharmacology, Yale University School of Medicine, 333 Cedar St., New Haven, CT, 06520, USA.

NPJ precision oncology

|July 21, 2023

概括

这项研究表明,结合FGFR和HDAC抑制剂,为患有FGFR3变异的膀癌 (BC) 提供了一个有前途的新治疗策略. 这种组合增强了erdafitinib的疗效,并可能导致对晚期BC进行新的临床试验.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
药理学药理学是指药理学的学科.

背景情况:

膀癌 (BC) 是一种常见的恶性瘤,频繁发生FGFR3变异.
目前的FGFR抑制剂,如erdafitinib显示有限的持久反应,需要新的治疗策略.
在BC病例的一个子集中,FGFR3的改变是关键驱动因素.

研究的目的:

为了研究结合FGFR抑制剂与基因素脱乙酶 (HDAC) 抑制剂的协同潜力,用于治疗BC.
在BC的临床前模型中探索这种协同作用的机制基础.
为FGFR3驱动的转移性BC患者确定新的治疗途径.

主要方法:

膀癌的体外和体外临床前模型.
使用厄尔达菲提尼布 (FGFR 抑制剂) 和奎西诺斯塔特 (HDAC 抑制剂) 的联合治疗.
评估FGFR3表达,翻译,HDGF水平和细胞活力.

主要成果:

在体外和体内证实了FGFR和HDAC抑制剂之间的协同作用.
奎西诺斯塔特通过抑制其翻译来抑制FGFR3的表达.
奎西诺斯塔特通过降低HDGF的调节,使BC细胞对erdafitinib敏感,包括具有FGFR3 S249C突变的细胞.

结论:

FGFR和HDAC抑制剂的组合代表了FGFR3驱动的BC的新和有效的治疗策略.
机理性洞察力揭示了基西诺斯塔特在降低FGFR3调节和使细胞对erdafitinib敏感方面的作用.
这些发现支持将这种联合治疗转化为膀癌早期临床试验.

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