PI3K/AKT/mTOR激活与状腺癌的恶性严重性和较差的预后有关
Jia-Xi Song1,2, Yong-Qiang Dong3, Ru-Lai Han1,2
1Department of Endocrine and Metabolic Diseases, Shanghai Institute of Endocrine and Metabolic Diseases, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
在甲状腺癌 (PCa) 中,PI3K/AKT/mTOR通路的激活与更高的恶性瘤和更差的存活率有关. 这种分子途径可能表明PCa的攻击性,影响患者的预后.
科学领域:
- 内分泌学 在内分泌学.
- 在瘤学瘤学.
- 分子生物学分子生物学
背景情况:
- 副甲状腺癌 (PCa) 是一种罕见的内分泌瘤,复发率高.
- 对于PCa预后的分子驱动因素尚不清楚.
- 研究PI3K/AKT/mTOR等特定的分子通路对于理解PCa行为至关重要.
研究的目的:
- 探索PI3K/AKT/mTOR通路激活在甲状腺癌中的重要性.
- 评估PI3K/AKT/mTOR激活与PCa患者的临床结果之间的相关性.
主要方法:
- 通过免疫组织化学分析了64名PCa患者和29名对照患者 (APT,PAd,PaN) 的mTORC1活性.
- 在66个PCa瘤组织中对PI3K/AKT/mTOR通路基因 (PIK3CA,PTEN,MTOR,TSC1,TSC2) 和CDC73进行了基因分析.
- 随访患者长达117个月,以评估无病存活率 (DFS) 和整体存活率 (OS).
主要成果:
- 与对照组相比,PCa中观察到显著升高的mTORC1活性.
- 48.5%的PCa瘤显示"高mTORC1"活性,而PAd/APT中的这一比例为22.7%.
- 在24.2%的PCa样本中检测到PI3K/AKT/mTOR变异;这些变异与较高的血清PTH,ALP,肌素以及显著较低的DFS和OS有关.
结论:
- 激活PI3K/AKT/mTOR通路是副甲状腺癌的一个重要分子特征.
- 这种途径的激活可能表明恶性瘤的程度,并预测PCa的不良结果.
- 针对PI3K/AKT/mTOR途径可能是PCa.的潜在治疗策略.
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