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:A timeline of tumour-associated macrophage biology.
A timeline of tumour-associated macrophage biology.
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肿瘤进展受局部微环境调控。该环境中存在大量免疫细胞,其中巨噬细胞是最丰富的细胞之一。临床相关性数据以及大量癌症小鼠模型的临床前研究表明,肿瘤相关巨噬细胞(TAM)发挥促癌作用。在原发肿瘤内,TAM促进肿瘤细胞侵袭和血管内渗以及肿瘤干细胞存活,并诱导血管生成。在转移部位,转移相关巨噬细胞促进外渗、肿瘤细胞存活和持续生长,并在某些情况下维持肿瘤细胞休眠。在原发部位和转移部位,TAM均抑制具有根除肿瘤潜力的细胞毒性T细胞和NK 细胞的活性。这些活性表明,TAM将成为治疗干预的主要靶点。在这篇Perspective文章中,我们按时间顺序探讨了我们对TAM生物学的理解演变,并将其置于巨噬细胞生物学重大推动性进展的背景中。
Tumour progression is modulated by the local microenvironment. This environment is populated by many immune cells, of which macrophages are among the most abundant. Clinical correlative data and a plethora of preclinical studies in mouse models of cancers have shown that tumour-associated macrophages (TAMs) play a cancer-promoting role. Within the primary tumour, TAMs promote tumour cell invasion and intravasation and tumour stem cell viability and induce angiogenesis.
At the metastatic site, metastasis-associated macrophages promote extravasation, tumour cell survival and persistent growth, as well as maintain tumour cell dormancy in some contexts. In both the primary and metastatic sites, TAMs are suppressive to the activities of cytotoxic T and natural killer cells that have the potential to eradicate tumours.
Such activities suggest that TAMs will be a major target for therapeutic intervention. In this Perspective article, we chronologically explore the evolution of our understanding of TAM biology put into the context of major enabling advances in macrophage biology.
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