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:Interactions between glioblastoma and myeloid cells.
Interactions between glioblastoma and myeloid cells.
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作为最具侵袭性的原发性恶性肿瘤,胶质母细胞瘤(GBM)具有显著的异质性,是胶质瘤治疗中的巨大挑战之一。髓系细胞,包括中性粒细胞、髓源性抑制细胞、小胶质细胞和巨噬细胞,在GBM的肿瘤微环境中发挥关键作用。在肿瘤微环境(TME)中,T细胞和自然杀伤(NK)细胞发挥抗肿瘤功能,而髓源性抑制细胞(MDSCs)可通过抑制这些免疫反应促进肿瘤进展。因此,MDSCs在塑造免疫治疗有效性方面发挥关键作用。TME限制了传统GBM治疗方法显著改善患者预后结局的能力。这一类方法涵盖手术切除和放射治疗等常规疗法,以及免疫治疗等前沿方法。通过对GBM微环境与肿瘤细胞之间动态相互作用的广泛研究,靶向治疗策略和创新免疫治疗模式均已出现,为临床干预提供了有前景的新方向。本综述聚焦于GBM与髓系细胞(MCs)之间的相互作用,为GBM的肿瘤发生和进展提供了新的见解。
Standing as the most aggressive form of primary malignant tumor, Glioblastoma (GBM) tumors with marked heterogeneity represents one of the enormous challenges in glioma treatment. Myeloid cells, which includes neutrophils, myeloid-derived suppressor cells, microglia, and macrophages, play a pivotal role in the tumor microenvironment of GBM.
In the tumor microenvironment (TME), T cells and natural killer (NK) cells exert anti-tumor functions, whereas myeloid-derived suppressor cells (MDSCs) can promote tumor progression by suppressing these immune responses.
Therefore, MDSCs play a critical role in shaping the effectiveness of immunotherapy. TME has constrained the ability of traditional GBM treatment approaches to significantly enhance prognostic outcomes for patients. This category encompasses conventional therapies like surgical resection and radiation therapy, along with cutting-edge methodologies such as immunotherapy.
Through extensive investigations into the dynamic interactions between the GBM microenvironment and neoplastic cells, both targeted treatment strategies and innovative immunotherapeutic modalities have emerged, offering promising new directions for clinical intervention. This review focuses on the interactions between GBM and myeloid cells (MCs), providing novel insights into the oncogenesis and progression of GBM.
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