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膀癌中的FGFR3变化:对向治疗的敏感性和耐药性

Maxim Noeraparast¹, Katarina Krajina¹, Renate Pichler²

¹Translational Oncology, II. Med Clinics Hematology and Oncology, Augsburg, Germany.

Cancer communications (London, England)

|August 20, 2024

概括

纤维细胞生长因子受体3 (FGFR3) 突变驱动膀癌 (BLCA) 并影响治疗反应. 了解耐药机制是开发有效的针对性治疗FGFR3突变BLCA的关键.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
癌症遗传学癌症遗传学

背景情况:

纤维细胞生长因子受体3 (FGFR3) 突变在膀癌 (BLCA) 中很普遍,影响瘤发生和瘤微环境 (TME).
在非肌肉侵入性和肌肉侵入性BLCA亚型中,FGFR3的改变至关重要.
表皮介质过渡 (EMT) 概况和TME状态对于预测FGFR3突变BLCA中对免疫检查点抑制剂的反应很重要.

研究的目的:

审查FGFR3在BLCA病原和治疗中的作用.
分析FGFR抑制剂的耐药性机制,如埃尔达菲提尼布.
探索新的治疗策略,包括FGFR3突变BLCA的组合治疗和合成致死性.

主要方法:

对临床前和临床证据的文献综述.
分析FGFR3突变状态及其对瘤生物学的影响.
研究耐药机制和潜在的治疗点.

主要成果:

FGFR3突变是BLCA的重要驱动因素,影响瘤开始和TME.
像埃尔达菲提尼布这样的FGFR抑制剂的疗效通常是短暂的,因为耐药性.
确定的抗性机制包括二次突变,表观遗传变化和表型异质性.

结论:

针对FGFR3突变BLCA的向治疗需要克服耐药性的策略.
组合治疗和合成杀伤性方法有望改善治疗结果.
对抗药机制的进一步研究对于在BLCA中推进个性化医学至关重要.

关键词:

膀癌:膀癌是一种癌症.埃尔达菲提尼布 (Erdafitinib) 是一种药物.抑制FGFR的抑制作用在FGFR3突变.对埃尔达菲提尼布的耐药性瘤微环境瘤微环境

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