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新辅助抗雄激素治疗与或没有MEK或SRC抑制不良风险前列腺癌:一期2随机临床试验

Raag Agrawal¹, Adam B Weiner², Julie Livingstone¹

¹Department of Human Genetics, David Geffen School of Medicine, University of California-Los Angeles, Los Angeles, CA, USA; Institute for Precision Health, University of California-Los Angeles, Los Angeles, CA, USA; Jonsson Comprehensive Cancer Center, University of California-Los Angeles, Los Angeles, CA, USA.

European urology oncology

|November 9, 2025

概括

抑制SRC或MEK途径并没有降低接受抗雄激素剥夺疗法 (ADT) 的前列腺癌患者的上皮细胞-介质细胞过渡 (EMT). 这种方法没有改善临床或病理结果,这表明它对缓解ADT耐药性的有效性不大.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
临床试验临床试验

背景情况:

前列腺癌中抗抗性素剥夺疗法 (ADT) 与上皮细胞-介质细胞过渡 (EMT) 有关.
SRC和MEK通路与驱动ADT耐药性和EMT有关.
针对这些途径是克服治疗耐药性的潜在策略.

研究的目的:

调查是否抑制SRC或MEK途径可以减少在接受ADT的前列腺癌患者的EMT.
评估SRC或MEK抑制对局部性前列腺腺癌的临床和病理结果的影响.

主要方法:

一个2期随机试验,涉及45名患有高风险前列腺腺癌的患者.
患者接受了新辅助ADT (甲胺+脱利克斯) 单独或与SRC抑制剂 (达沙替尼布) 或MEK抑制剂 (特拉美替尼布) 联合.
主要终点:通过免疫组织化学 (IHC) 的EMT标记物 (N-cadherin,vimentin) 的丰富性;次要终点:临床病理学结果,安全性.

主要成果:

在治疗臂之间,IHC对N-cadherin和vimentin表达没有显著差异.
在生化复发,恢复或最小残留疾病的时间内没有观察到任何改善.
在所有手臂中观察到MAP2K1,MAP2K2和SRCRNA水平的显著下降;没有3级以上的不良事件.

结论:

新辅助抑制SRC或MEK通路不会减轻前列腺癌中EMT对ADT的反应.
这种治疗策略没有影响关键的临床或病理结果.
与ADT一起准SRC/MEK途径对于改善该患者群体的结果是无效的.

关键词:

年龄年龄年龄年龄年龄年龄激素对抗剂激素对抗剂抗瘤药剂是一种抗瘤药剂.达沙替尼布 (Dasatinib) 是一种皮质-介质细胞过渡.基因表达调节基因表达调节在MAP激酶信号传递中.新辅助疗法是一种新辅助疗法.前列腺切除术是指前列腺切除术.前列腺新生体前列腺瘤.

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