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三阴性乳腺癌中的免疫检查点阻断:现状与耐药的分子机制

Immune Checkpoint Blockades in Triple-Negative Breast Cancer: Current State and Molecular Mechanisms of Resistance.

作者信息

Kim Hyungjoo, Choi Je-Min, Lee Kyung-Min

机构信息

Department of Life Science, College of Natural Sciences, Hanyang University, Seoul 04763, Korea.

Penta Medix Co., Ltd., Seongnam-si 13449, Korea.

出版信息

Biomedicines. 2022 May 13;10(5):1130. doi: 10.3390/biomedicines10051130.

DOI:10.3390/biomedicines10051130
PMID:35625867
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9138553/
Abstract

Immune checkpoint blockades (ICBs) have revolutionized cancer treatment. Recent studies have revealed a subset of triple-negative breast cancer (TNBC) to be considered as an immunogenic breast cancer subtype. Characteristics of TNBC, such as higher mutation rates and number of tumor-infiltrating immune cells, render the immunogenic phenotypes. Consequently, TNBCs have shown durable responses to ICBs such as atezolizumab and pembrolizumab in clinic. However, a significant number of TNBC patients do not benefit from these therapies, and mechanisms of resistance are poorly understood. Here, we review biomarkers that predict the responsiveness of TNBCs to ICB and recent advances in delineating molecular mechanisms of resistance to ICBs.

摘要

免疫检查点阻断(ICB)彻底改变了癌症治疗方式。最近的研究表明,三阴性乳腺癌(TNBC)的一个亚群可被视为免疫原性乳腺癌亚型。TNBC的特征,如较高的突变率和肿瘤浸润免疫细胞数量,造就了其免疫原性表型。因此,TNBC在临床上已显示出对阿特珠单抗和帕博利珠单抗等ICB有持久反应。然而,相当数量的TNBC患者并未从这些治疗中获益,且耐药机制尚不清楚。在此,我们综述了预测TNBC对ICB反应性的生物标志物以及在阐明ICB耐药分子机制方面的最新进展。

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本文引用的文献

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In vivo CRISPR screens identify the E3 ligase Cop1 as a modulator of macrophage infiltration and cancer immunotherapy target.体内 CRISPR 筛选鉴定出 E3 连接酶 Cop1 作为巨噬细胞浸润的调节剂和癌症免疫治疗靶点。
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AIbZIP/CREB3L4 Promotes Cell Proliferation via the SKP2-p27 Axis in Luminal Androgen Receptor Subtype Triple-Negative Breast Cancer.AIbZIP/CREB3L4 通过 SKP2-p27 轴促进腔面雄激素受体亚型三阴性乳腺癌中的细胞增殖。
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