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:CD24: A Novel Target for Cancer Immunotherapy.
CD24: A Novel Target for Cancer Immunotherapy.
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分化簇24(CD24)是一种体积较小、高度糖基化的细胞黏附蛋白,正常情况下表达于免疫细胞以及上皮、神经和肌肉细胞。肿瘤中CD24的表达与多条致癌信号通路的改变有关。此外,CD24与Siglec-10的相互作用可能参与肿瘤免疫逃逸,抑制巨噬细胞介导的吞噬作用及自然杀伤(NK)细胞的细胞毒活性。临床前研究中,阻断CD24已显示出良好前景。尽管疗效数据有限,抗CD24单克隆抗体已在两项临床试验中显示出安全性和良好耐受性。临床前评估的其他治疗方式还包括抗体偶联药物和嵌合抗原受体(CAR)T细胞治疗。本文总结CD24作为癌症免疫治疗潜在靶点的现有证据及未来展望。
Cluster of differentiation 24 (CD24) is a small, highly glycosylated cell adhesion protein that is normally expressed by immune as well as epithelial, neural, and muscle cells. Tumor CD24 expression has been linked with alterations in several oncogenic signaling pathways.
In addition, the CD24/Siglec-10 interaction has been implicated in tumor immune evasion, inhibiting macrophage-mediated phagocytosis as well as natural killer (NK) cell cytotoxicity. CD24 blockade has shown promising results in preclinical studies. Although there are limited data on efficacy, monoclonal antibodies against CD24 have demonstrated clinical safety and tolerability in two clinical trials.
Other treatment modalities evaluated in the preclinical setting include antibody-drug conjugates and chimeric antigen receptor (CAR) T cell therapy. In this review, we summarize current evidence and future perspectives on CD24 as a potential target for cancer immunotherapy.
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