手术应激诱导的肿瘤免疫抑制环境。

IF 3.3 3区 医学 Q2 ONCOLOGY
Fan Yang, Qing Hua, Xiaoyan Zhu, Pingbo Xu
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引用次数: 0

摘要

尽管几十年来癌症治疗取得了重大进展,但手术切除仍是实体瘤的主要治疗方法。不幸的是,越来越多的证据表明,肿瘤切除造成的手术应激有可能引发术后转移龛的形成。手术应激不仅会激活交感-肾上腺髓质轴和下丘脑-垂体-肾上腺皮质轴,还会诱发缺氧和高凝状态。这些不利因素会通过下调免疫效应细胞和上调免疫抑制细胞对免疫系统产生负面影响,从而导致术后肿瘤转移龛的定植和进展。本综述总结了手术应激对四种免疫效应细胞(中性粒细胞、巨噬细胞、自然杀伤细胞和细胞毒性 T 淋巴细胞)和两种免疫抑制细胞(调节性 T 细胞和髓源性抑制细胞)的影响,并讨论了术后肿瘤复发和进展的免疫机制。此外,还阐明了相关的治疗策略,以尽量减少手术应激的促肿瘤效应。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Surgical stress induced tumor immune suppressive environment.

Despite significant advances in cancer treatment over the decades, surgical resection remains a prominent management approach for solid neoplasms. Unfortunately, accumulating evidence suggests that surgical stress caused by tumor resection may potentially trigger postoperative metastatic niche formation. Surgical stress not only activates the sympathetic-adrenomedullary axis and hypothalamic-pituitary-adrenocortical axis but also induces hypoxia and hypercoagulable state. These adverse factors can negatively impact the immune system by downregulating immune effector cells and upregulating immune suppressor cells, which contribute to the colonization and progression of postoperative tumor metastatic niche. This review summarizes the effects of surgical stress on four types of immune effector cells (neutrophils, macrophages, natural killer cells and cytotoxic T lymphocytes) and two types of immunosuppressive cells (regulatory T cells and myeloid-derived suppressor cells), and discusses the immune mechanisms of postoperative tumor relapse and progression. Additionally, relevant therapeutic strategies to minimize the pro-tumorigenic effects of surgical stress are elucidated.

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来源期刊
Carcinogenesis
Carcinogenesis 医学-肿瘤学
CiteScore
9.20
自引率
2.10%
发文量
95
审稿时长
1 months
期刊介绍: Carcinogenesis: Integrative Cancer Research is a multi-disciplinary journal that brings together all the varied aspects of research that will ultimately lead to the prevention of cancer in man. The journal publishes papers that warrant prompt publication in the areas of Biology, Genetics and Epigenetics (including the processes of promotion, progression, signal transduction, apoptosis, genomic instability, growth factors, cell and molecular biology, mutation, DNA repair, genetics, etc.), Cancer Biomarkers and Molecular Epidemiology (including genetic predisposition to cancer, and epidemiology), Inflammation, Microenvironment and Prevention (including molecular dosimetry, chemoprevention, nutrition and cancer, etc.), and Carcinogenesis (including oncogenes and tumor suppressor genes in carcinogenesis, therapy resistance of solid tumors, cancer mouse models, apoptosis and senescence, novel therapeutic targets and cancer drugs).
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