炎症驱动的基因组不稳定性:通往癌症发展和治疗耐药性的途径
Nina Rembiałkowska1, Zofia Kocik2, Amelia Kłosińska2
1Department of Molecular and Cellular Biology, Faculty of Pharmacy, Wroclaw Medical University, Borowska 211A, 50-556 Wroclaw, Poland.
Pharmaceuticals (Basel, Switzerland)
|September 27, 2025
概括
慢性炎症通过导致DNA损伤和阻碍修复来驱动癌症. 用像NSAIDs这样的药物向炎症提供了有前途的癌症预防和治疗策略.
科学领域:
- 在瘤学瘤学.
- 免疫学 免疫学 免疫学
- 分子生物学分子生物学
背景情况:
- 慢性炎症是一种生理反应,是癌症发展的重要因素.
- 持续的炎症信号产生反应性氧和物种 (ROS/RNS),导致DNA损伤.
- 促炎媒介和免疫细胞创造了一个促进瘤的微环境和基因组不稳定性.
研究的目的:
- 阐明慢性炎症在致癌和治疗耐药性中的作用.
- 探索炎症诱导基因组不稳定的机制.
- 评估抗炎药物在癌症预防和治疗中的潜力.
主要方法:
- 审查有关炎症,DNA损伤和癌症的现有文献.
- 分析参与炎症诱导的基因组不稳定性的信号通路 (例如NF-κB,IL-6,TNF-α).
- 检查免疫细胞对瘤微环境的影响.
- 评估炎症在化疗和放射性耐药性中的作用.
主要成果:
- 慢性炎症通过导致DNA损伤和破坏DNA修复来促进癌症.
- 炎症媒介和免疫细胞有助于基因组不稳定性和亲瘤原生环境.
- 炎症调节DNA损伤反应通路,可能导致治疗抵抗.
- 抗炎药物 (NSAIDs,皮质类固醇,单克隆抗体) 在临床前和临床环境中显示出癌症预防和治疗的前景.
结论:
- 慢性炎症是癌症发病和进展的关键驱动因素.
- 准炎症途径是预防和治疗癌症的可行策略.
- 进一步的临床评估是必要的,以优化抗炎药物的使用,因为潜在的不良影响.
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