RNF43 p.G659fs 通过 PI3K/AKT/mTOR 信号通路和 HLA-E 上调导致 MSI-high 结直肠癌中 NK 细胞功能障碍
RNF43 p.G659fs leads to natural killer cell dysfunction in MSI-high colorectal cancer through PI3K/AKT/mTOR signaling and HLA-E up-regulation.
CELL INTELLIGENCE · 肿瘤细胞治疗研究
肿瘤细胞治疗研究
患者来源的卵巢癌类器官平台用于研究对 NK 细胞的易感性
英文原题：A patient-derived ovarian cancer organoid platform to study susceptibility to natural killer cells.
查看英文原题
A patient-derived ovarian cancer organoid platform to study susceptibility to natural killer cells.
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中文摘要
肿瘤内异质性驱动晚期癌症（如卵巢癌）的治疗耐药和复发。在此，我们提出一种使用患者来源卵巢癌类器官的活细胞成像检测方法，可同时实时捕获并定量500多个类器官中NK 细胞介导的凋亡事件。我们的检测揭示了显著的肿瘤间和肿瘤内应答异质性，并鉴定出一个罕见的耐药类器官群体，为测试克服耐药的免疫调节策略开辟了途径。
展开英文摘要原文
Intratumoral heterogeneity drives therapy resistance and relapses in advanced stage cancers, such as ovarian cancer.
Here, we present a live cell imaging assay using patient-derived ovarian cancer organoids for real time capture and quantification of natural killer cell-mediated apoptotic events in >500 organoids simultaneously.
Our assay revealed significant inter- and intratumor response heterogeneity and identified a rare resistant organoid population, opening avenues to test immunomodulatory strategies that overcome resistance.
论文信息
- 作者
- Mercadante M、Scheben A、Estrada J、Savas-Carstens J、Sullivan W、Housel N、Volpari T、Hebner J
- 单位
- The New York Stem Cell Foundation Research Institute, New York, NY.United States
- 文献类型
- 预印本
- 期刊
- bioRxiv : the preprint server for biology2025 Mar 7
- 原文标识
- PubMed 40093054 · DOI 10.1101/2025.03.06.641285