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:Blocking HIF to Enhance NK Cells: Hints for New Anti-Tumor Therapeutic Strategies?
Blocking HIF to Enhance NK Cells: Hints for New Anti-Tumor Therapeutic Strategies?
分数与星级只用于站内排序 —— 不代表疗效、安全性或个人适用性。
自然杀伤(NK)细胞正逐渐成为开发新型抗肿瘤策略的有前景工具。然而,要获得通用且有效的NK细胞疗法,仍面临两大挑战:如何最大程度延长患者体内强效NK效应细胞的持久性,以及如何克服使NK细胞无法进入或在肿瘤部位受到抑制的多种逃逸机制。在此方面,靶向缺氧诱导因子(HIF)可能带来机会,因为HIF对肿瘤进展和免疫抑制都很重要,尤其是在当前旨在开发更有效NK细胞治疗产品的研究背景下。
Natural Killer (NK) cells are becoming an ever more promising tool to design new anti-tumor strategies.
However, two major issues are still a challenge to obtain versatile and effective NK-based therapies: the way to maximize the persistency of powerful NK effectors in the patient, and the way to overcome the multiple escape mechanisms that keep away or suppress NK cells at the tumor site. In this regard, targeting the hypoxia-inducible factors (HIFs), which is important for both tumor progression and immune suppression, may be an opportunity. Especially, in the context of the ongoing studies focused on more effective NK-based therapeutic products.
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