融合阳性甲状腺癌:从诊断到向治疗
Vicente R Marczyk1, Sasan Fazeli1, Ramona Dadu1
1Department of Endocrine Neoplasia and Hormonal Disorders, The University of Texas MD Anderson Cancer, Houston, TX.
JCO precision oncology
|February 21, 2025
概括
神经断性热氨酸受体激酶 (NTRK) 融合驱动甲状腺癌. 针对性治疗的耐药性通常涉及NTRK溶剂前端突变,特别是在晚期甲状腺癌中,需要谨慎使用TRK抑制剂.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 遗传学 遗传学 是一个
背景情况:
- 神经断性热氨酸受体激酶 (NTRK) 融合可以驱动甲状腺癌.
- 关于这些罕见的融合的临床,病理和分子特征以及它们对向治疗的反应的数据有限.
研究的目的:
- 分析NTRK融合阳性甲状腺癌的临床,病理和分子特征.
- 调查患者对向治疗的反应,并确定耐药性机制.
主要方法:
- 在一个单一的美国癌症中心进行了回顾性观察研究.
- 包括65名患有NTRK融合阳性甲状腺癌 (成人和儿科) 的患者.
- 对临床数据,病理特征和分子变化的分析,包括耐药性突变.
主要成果:
- 在乳头,差差分化和形甲状腺癌中确定了NTRK融合.
- 在41%的乳头甲状腺癌中观察到毛囊生长模式.
- 新出现的NTRK溶剂前端突变 (G623R,G595R) 在PDTC/ATC中导致对larotrectinib的耐药性.
- 观察到塞利特雷克提尼布的部分反应,但对形甲状腺癌患者在一年内进展.
结论:
- 在各种甲状腺癌亚型中存在NTRK1/3融合,通常具有卵泡生长模式.
- NTRK溶剂前端突变是对TRK抑制剂的关键抵抗机制,特别是在PDTC/ATC中.
- 单剂TRK抑制剂的疗效在厌塑性甲状腺癌中是有限的,因此需要谨慎的临床应用.
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There are several types of targeted therapies against specific...
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