重编程先天免疫力以克服雌激素受体阳性乳腺癌中的内分泌抵抗
Siti Nur Hasyila Muhammad1, Maryam Azlan2, Agustine Nengsih Fauzi1,3
1Department of Chemical Pathology, School of Medical Sciences, Universiti Sains Malaysia, Kubang Kerian, Kelantan, Malaysia.
International journal of cancer
|March 7, 2026
概括
瘤微环境中的先天性免疫细胞通过STAT3途径抑制抗瘤免疫力,驱动ER+乳腺癌中的内分泌抵抗. 抑制STAT3可能会恢复对内分泌疗法的敏感性.
科学领域:
- 在瘤学瘤学.
- 免疫学 免疫学 免疫学
- 内分泌学 在内分泌学.
背景情况:
- 雌激素受体阳性 (ER+) 乳腺癌是常见的,但内分泌治疗的疗效受到耐药性和复发的限制.
- 虽然已知瘤内在因素,但瘤微环境 (TME) 和先天性免疫细胞显著影响治疗结果.
- 了解这些免疫相互作用对于克服内分泌抵抗至关重要.
研究的目的:
- 审查TME中的先天性免疫细胞如何促进ER+乳腺癌中的内分泌抵抗.
- 阐明STAT3信号通路在调解免疫失调和治疗耐药性的作用.
- 探索针对STAT3的治疗潜力,并将内分泌疗法与免疫调节结合起来.
主要方法:
- 文献综述综合了与乳腺癌相关的免疫学和内分泌学的最新进展.
- 对研究内分泌耐药模型中STAT3抑制的临床前研究的分析.
- 检查先天免疫细胞 (TAMs,NK细胞,MDSCs,TANs) 和TME之间的交叉关系.
主要成果:
- 天生的免疫细胞培养一种免疫抑制的TME,破坏了ER+乳腺癌中的内分泌反应能力.
- STAT3信号通路集成压力信号,驱动免疫重编程,并促进治疗抵抗.
- 在临床前模型中,STAT3抑制显示出恢复他莫西芬敏感性的潜力.
结论:
- 天生的免疫细胞和STAT3通路是ER+乳腺癌内分泌抵抗的关键参与者.
- 向STAT3并将内分泌疗法与免疫调节相结合,提供了一个有前途的治疗策略.
- 未来的方法可能涉及STAT3抑制剂,免疫检查点阻塞和个性化治疗的生物标志物.
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