肥胖,慢性乳腺炎和致癌:分子途径和临床影响 (综述)
1First Clinical Medical College of Gansu University of Chinese Medicine, Lanzhou, Gansu 730000, P.R. China.
International journal of oncology
|November 28, 2025
概括
肥胖增加了乳腺癌的风险和死亡率,通过促进慢性炎症和激活瘤性途径. 了解这些分子联系对于为肥胖患者开发有针对性的预防和精确瘤学策略至关重要.
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:
- 肥胖是一个全球性流行病,与更高的乳腺癌 (BC) 风险和死亡率有关,特别是在绝经后的妇女中.
- 肥胖引起的炎症,失调的阿迪波基因 (莱普丁,阿迪波内克丁),胰岛素耐药性和细胞因子 (TNF-α,IL-6) 驱动BC的发展.
- 这些因素激活致癌途径 (NF-κB,PI3K/AKT/mTOR),导致DNA损伤,增殖和免疫抑制.
研究的目的:
- 审查有关肥胖,炎症和乳腺癌相关的分子机制的现有证据.
- 探索这些相互作用对BC患者的临床影响.
- 在肥胖个体中为BC预防和精确瘤学的策略提供信息.
主要方法:
- 文献综述综合当前的科学证据.
- 对参与肥胖相关乳腺癌发生的分子途径的分析.
- 检查与BC呈现和结果相关的临床数据.
主要成果:
- 肥胖通过慢性炎症,改变信号传递和激活致癌途径促进乳腺癌.
- 肥胖的BC患者经常出现晚期瘤,治疗反应较差,生存率降低.
- 目前对肥胖-BC分子相互作用的理解需要进一步阐明,以改善诊断和预后.
结论:
- 与肥胖相关的炎症是乳腺癌发展和进展的关键驱动因素.
- 需要对分子机制进行进一步的研究,以完善肥胖BC患者的诊断和预后工具.
- 翻译性研究可以为有针对性的预防和精确瘤学策略提供信息,以改善这一群体的结果.
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