时间标签：数据日期 2026-10-31 · 生成时间 2026-11-01 05:30（Asia/Shanghai）｜ 检索窗口 PubMed edat 2026/10/28–2026/10/31 ｜ 情报发生日期 2026-10-31
证据级别：摘要级。本条依据 PubMed 结构化摘要与元数据撰写，付费墙全文未获取、未逐节核验，本站未做任何数值推算补全。
研究问题
The polarization of macrophages and the deactivation of oncogenic pathways within the tumor microenvironment are directly linked to the evolution of hepatocellular carcinoma (HCC), a relatively frequent cancer in the world. Though the exact mechanism is yet unknown, tumor-associated macrophages (TAMs) may alter p53 activity by secreting cytokines. In contrast, the (tumor protein p53, p53) signaling pathway is frequently functionally compromised in HCC as a result of mutation or epigenetic silencing. It is yet unknown if the natural substance luteolin restores p53 function by controlling macrophage polarization, despite its multi-targeted anti-tumor potential.
局限
未能获取全文，具体设计细节、失访与统计学处理无法核验。
对本项目的价值
★☆☆☆☆ 相关范围内，作为背景与横向对照收录。设计 single-cell。
原文题录
- 英文标题：Correlative insights into luteolin regulating the macrophage-p53-CCNB1/CDK1 axis associated with cell-cycle control in hepatocellular carcinoma.
- 期刊与标识：Biochem Biophys Res Commun · PMID 42950621 · DOI 10.1016/j.bbrc.2026.154768
B 级证据分级：B 级（同行评议临床前研究，主要为动物模型）
本文核心结论来自动物模型或体外细胞学，属临床前证据，不能外推至人体。「延长健康寿命」「改善功能」等表述在小鼠中的意义，与人类临床结局之间仍有距离。
关于本文的文献来源：本站依据 IMA 知识库「五刊监控·深度文献卡片」（SOP §4.2 摘要级）撰写，依据期刊公开摘要与 PubMed 元数据；付费墙全文未获取之处已标注「待补全文」，未做任何数值推算补全。