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:TIGIT in Lung Cancer: Potential Theranostic Implications.
TIGIT in Lung Cancer: Potential Theranostic Implications.
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TIGIT(T细胞免疫受体,具有Ig和ITIM结构域)是一种共抑制受体,表达于多种免疫细胞,包括T细胞、NK细胞和树突状细胞。TIGIT与不同配体相互作用,如CD155和CD112,这些配体在癌细胞上高表达,导致免疫应答抑制。近期研究强调了TIGIT在肿瘤微环境中调节免疫细胞功能的重要性及其作为潜在治疗靶点的作用,尤其是在肺癌领域。然而,TIGIT在癌症发生和进展中的作用仍存在争议,特别是关于其在肿瘤微环境和肿瘤细胞上表达的相关性,其预后和预测意义迄今基本上尚未明确。在此,我们综述了TIGIT阻断在肺癌中的最新进展,并对TIGIT作为免疫组化生物标志物的相关性及其可能的诊疗一体化意义提供了见解。
TIGIT (T cell immunoreceptor with Ig and ITIM domains) is a co-inhibitory receptor expressed on various immune cells, including T cells, NK cells, and dendritic cells. TIGIT interacts with different ligands, such as CD155 and CD112, which are highly expressed on cancer cells, leading to the suppression of immune responses. Recent studies have highlighted the importance of TIGIT in regulating immune cell function in the tumor microenvironment and its role as a potential therapeutic target, especially in the field of lung cancer.
However, the role of TIGIT in cancer development and progression remains controversial, particularly regarding the relevance of its expression both in the tumor microenvironment and on tumor cells, with prognostic and predictive implications that remain to date essentially undisclosed.
Here, we provide a review of the recent advances in TIGIT-blockade in lung cancer, and also insights on TIGIT relevance as an immunohistochemical biomarker and its possible theranostic implications.
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