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瘤亚型,PPARγ表达和脂肪增殖之间的相互作用形成了乳腺癌的结果

Aditya Shah^1,2, Katie Liu^1,3, Ryan Liu^1,4

¹Departments of Cellular & Molecular Physiology, Internal Medicine (Endocrinology), and Comparative Medicine, Yale University, New Haven, CT, United States.

medRxiv : the preprint server for health sciences

|July 17, 2025

概括

高PPARγ基因表达表明更好的乳腺癌存活率,特别是在绝经前妇女. 脂肪组织的增殖因瘤亚型而异,这表明有针对性的疗法.

科学领域:

在瘤学瘤学.
代谢研究研究代谢研究
遗传学是一个遗传学.

背景情况:

乳腺癌的进展是复杂的,受瘤生物学,患者的新陈代谢和更年期状态的影响.
过氧体增殖器激活受体玛 (PPARγ) 是脂质代谢的关键调节器,在癌症中可能发挥作用.
脂肪组织的代谢活性可能与乳腺癌亚型和患者特征相关.

研究的目的:

研究PPARγ基因表达在乳腺癌中的预后意义.
探索PPARγ表达,绝经状态和乳腺癌存活率之间的关系.
检查与乳腺癌亚型和患者表型有关的脂肪组织增殖标志物.

主要方法:

来自TCGA-BRCA队列 (n=1094) 的RNA测序数据的分析,按PPARγ表达,更年期状态和瘤受体状态 (ER+,HER2-,TNBC) 分层分层.
卡普兰-梅尔生存分析,以评估高PPARγ表达和整体/疾病特异性生存之间的关联.
对PET-CT扫描 (ACRIN-6888试验,n=69) 的分析,测量不同患者和瘤亚组的脂肪组织中18F-FLT吸收 (SUV指标).

主要成果:

高PPARγ表达 (≥6.903 FPKM) 与改善整体和疾病特异性生存率显著相关,特别是在绝经前患者中.
绝经后的患者与绝经前的患者相比,表现出较低的内脏脂肪组织SUV平均值.
ER+和非TNBC瘤与显著较低的脂肪组织SUVpeak和SUVmax有关,这表明代谢重编程.

结论:

PPARγ是乳腺癌的潜在治疗标,调节脂质代谢并影响患者的治疗结果.
脂肪组织增殖和代谢活动根据乳腺癌亚型和患者更年期状态进行重新编程.
这些发现支持开发针对乳腺癌代谢途径的亚型特定治疗策略.

关键词:

在18F-FLT.在PPARγ中,PPARγ是PPARγ 脂肪组织的脂肪组织.乳腺癌乳腺癌乳腺癌脂质脂质脂质是一种

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