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
英文原题:Engineering and targeting potential of CAR NK cells in colorectal cancer.
Engineering and targeting potential of CAR NK cells in colorectal cancer.
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结直肠癌(CRC)是全球重要的健康问题,亟需创新疗法。嵌合抗原受体(CAR)T细胞已显示出治疗前景,但仍面临挑战。越来越受关注的是CAR自然杀伤(NK)细胞,其优势包括安全性较高、成本效益较好,以及对实体瘤具有疗效。然而,CAR-NK细胞迁移的具体机制及其在复杂肿瘤微环境中的相互作用仍需深入研究。本文介绍CAR-NK细胞的设计与工程化改造、CRC中的抗原靶点,以及克服耐药机制方面的进展,并重点讨论其临床试验潜力。
Colorectal cancer (CRC), a major global health concern, necessitates innovative treatments. Chimeric antigen receptor (CAR) T cells have shown promises, yet they grapple with challenges. The spotlight pivots to the rising heroes: CAR natural killer (NK) cells, offering advantages such as higher safety profiles, cost-effectiveness, and efficacy against solid tumors. Nevertheless, the specific mechanisms underlying CAR NK cell trafficking and their interplay within the complex tumor microenvironment require further in-depth exploration.
Herein, we provide insights into the design and engineering of CAR NK cells, antigen targets in CRC, and success in overcoming resistance mechanisms with an emphasis on the potential for clinical trials.
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