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:Tumor immune microenvironment remodeling after neoadjuvant therapy in gastric cancer: Update and new challenges.
Tumor immune microenvironment remodeling after neoadjuvant therapy in gastric cancer: Update and new challenges.
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胃癌(GC)是全球发病率和死亡率最高的恶性肿瘤之一。新辅助治疗,包括新辅助化疗(NAC)和NAC联合免疫治疗,可以提高切除率和长期生存率。然而,并非所有患者对新辅助治疗都有良好反应。已证实肿瘤免疫微环境中的免疫细胞,包括T细胞、B细胞和NK 细胞,可影响新辅助治疗的疗效。本文总结了当前的临床前和临床证据,以更全面地描述新辅助治疗对GC免疫微环境的影响,为识别预测新辅助治疗疗效的生物标志物提供动力,并揭示耐药机制,从而促进GC患者个体化和精准治疗的发展。
Gastric cancer (GC) is a malignant tumor with one of the highest morbidity and death rates in the world. Neoadjuvant therapy, including neoadjuvant chemotherapy (NAC) and NAC combined with immunotherapy, can improve the resection and long-term survival rates.
However, not all patients respond well to neoadjuvant therapy. It has been confirmed that immune cells in the tumor immune microenvironment, including T cells, B cells, and natural killer cells, can affect the efficacy of neoadjuvant therapy.
This paper summarizes current preclinical and clinical evidence to more fully describe the effects of neoadjuvant therapy on the immune microenvironment of GC, to provide the impetus to identify biomarkers to predict the potency of neoadjuvant therapy, and to identify the mechanisms of drug resistance, which should promote the development of individualized and accurate treatments for GC patients.
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