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耐药性的隐藏结构:黑色素瘤免疫景观中的细胞外基质

英文原题:Hidden architecture of resistance: The extracellular matrix in melanoma's immune landscape.

PubMed 2026/06/12(内容时间) Semin Cancer Biol Q1 · IF 20.3(JCR 2025)

研究概要

皮肤黑色素瘤(CM)的肿瘤异质性归因于肿瘤细胞、免疫细胞和肿瘤基质在功能和结构上的多样性,并决定患者对治疗的反应。

中文摘要

皮肤黑色素瘤(CM)的肿瘤异质性归因于肿瘤细胞、免疫细胞和肿瘤基质在功能和结构上的多样性,并决定患者对治疗的反应。肿瘤免疫微环境(TIME)由多种细胞和非细胞成分组成。细胞包括癌症相关成纤维细胞、T细胞、NK细胞、B细胞、树突状细胞、髓源性抑制细胞和单核细胞。非细胞成分包括细胞因子、生长因子和细胞外基质(ECM)。在本综述中,我们特别关注ECM分子,即胶原蛋白、纤连蛋白、层粘连蛋白、透明质酸、半乳糖凝集素和基质金属蛋白酶,在塑造黑色素瘤TIME中的关键作用。我们通过考察ECM成分的物理特性和生物学功能如何调节癌症与免疫细胞之间的相互作用来探讨这些成分,从而影响黑色素瘤中的免疫并强调其临床意义。

展开英文摘要原文

Tumor heterogeneity in cutaneous melanoma (CM) is attributed to the functional and structural diversity of tumor cells, immune cells, and the tumor stroma, and determines patients' response to therapy. The tumor immune microenvironment (TIME) comprises a diverse array of cellular and non-cellular components. Cells include cancer-associated fibroblasts, T cells, NK cells, B cells, dendritic cells, myeloid-derived suppressor cells, and monocytes. Non-cellular components include cytokines, growth factors, and extracellular matrix (ECM). In this review, we specifically focus on the critical roles of ECM molecules, namely collagen, fibronectin, laminin, hyaluronic acid, galectin, and matrix metalloproteinase, in shaping the melanoma TIME. We explore ECM components by examining how their physical properties and biological functions regulate the interactions between cancer and immune cells, thereby impacting immunity in melanoma and underscoring their clinical significance.

论文信息

作者
Guan Y、Edny G、Chandra J、Souza-Fonseca-Guimaraes F、Haass NK
第一作者单位
Frazer Institute, Faculty of Health, Medicine and Behavioural Sciences, The University of Queensland, Woolloongabba, QLD 4102, Australia.Australia
通讯作者单位
Frazer Institute, Faculty of Health, Medicine and Behavioural Sciences, The University of Queensland, Woolloongabba, QLD 4102, Australia. Electronic address: n.haass1@uq.edu.au.Australia
文献类型
综述
期刊
Seminars in cancer biology2026 Sep
原文标识
PubMed 42285239 · DOI 10.1016/j.semcancer.2026.06.004