在ROS1融合阳性癌症中,TKI类型切换克服了ROS1 L2086F
bioRxiv : the preprint server for biology
|January 31, 2024
概括
在非小细胞肺癌中,ROS1 L2086F突变赋予了对I型氨酸激酶抑制剂 (TKI) 的耐药性. II型TKI卡博桑提尼布和I型FLT3抑制剂吉尔特利尼布对这些耐药突变显示出有效性.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 药物发现 药物发现 药物发现
背景情况:
- 氨酸激酶抑制剂 (TKI) 对ROS1阳性非小细胞肺癌 (NSCLC) 有效.
- 对TKI的获得性耐药性限制了治疗的耐久性.
- 下一代ROS1 TKI的阻力机制尚未得到充分理解.
结论:
- 卡博桑提尼布和吉尔特里尼布对ROS1 L2086F突变是有效的.
- 卡博桑提尼布在耐TCI的ROS1 L2086FNSCLC患者中表现出临床活性.
- 吉尔特里尼布是一种潜在的替代治疗选择.
- 持续需要更有选择性和更好耐受的TKI来克服像ROS1 L2086F.这样的内在耐药性突变.
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