在驱动前列腺癌治疗耐药性的治疗诱导的干和血统可塑性
Anmbreen Jamroze1, Xiaozhuo Liu1, Dean G Tang1,2
1Department of Pharmacology & Therapeutics, Roswell Park Comprehensive Cancer Center, Buffalo, NY 14263, USA.
Cancer heterogeneity and plasticity
|October 4, 2024
概括
癌细胞的异质性推动了对TKI和ARSI等疗法的耐药性. 治疗可以诱导癌细胞谱系的可塑性,促进进一步的耐药性,特别是在前列腺癌中.
科学领域:
- 在瘤学瘤学.
- 癌症生物学 癌症生物学
- 分子治疗学分子治疗学
背景情况:
- 癌细胞在表观遗传和转录状态中表现出异质性,影响表型,功能和药物敏感性.
- 这种异质性有助于瘤抵抗向疗法,包括氨酸激酶抑制剂 (TKI) 和雄激素受体信号传导抑制剂 (ARSI).
- 治疗干预可以诱导癌细胞的血统可塑性或不忠,进一步加剧治疗耐药性.
研究的目的:
- 讨论癌细胞谱系的可塑性,重点关注治疗诱导的切换到基底/干状,介质和神经谱系.
- 使用前列腺癌 (PCa) 作为一个模型,以说明抗受体信号传递抑制剂 (ARSI) 诱导的血统可塑性在割耐药PCa (CRPC) 发育中.
- 探索瘤微环境 (TME) 对治疗诱导的血统可塑性的影响,并总结其调节器和机制.
主要方法:
- 关于癌细胞异质性和谱系可塑性的当前文献的审查和综合.
- 专注于前列腺癌作为ARSI诱导的血统不忠的案例研究.
- 讨论瘤微环境 (TME) 的作用和关键的调节机制.
主要成果:
- 癌细胞异质性是癌症治疗的一个基本挑战,导致抗性.
- 治疗方法,特别是前列腺癌中的ARSIs,可以诱导癌细胞系的切换,从而导致抵抗割的前列腺癌 (CRPC).
- 瘤微环境 (TME) 在调节治疗诱导的血统可塑性方面发挥着重要作用.
结论:
- 了解和准癌症细胞系不忠的调节者对于改善治疗结果至关重要.
- 针对谱系可塑性提供了一种潜在的策略,以克服治疗耐药性并延长治疗窗口.
- 对推动血统不忠的机制的进一步研究可以导致新的治疗方法,以提高患者的生存率.
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