• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

癌症免疫疗法反应和抵抗的转录决定因素。

Transcriptional determinants of cancer immunotherapy response and resistance.

机构信息

Department of Biochemistry and Molecular Genetics, University of Alabama at Birmingham, Birmingham, AL 35233, USA; O'Neal Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL 35233, USA.

O'Neal Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL 35233, USA; Division of Hematology and Oncology, University of Alabama at Birmingham, Birmingham, AL, USA.

出版信息

Trends Cancer. 2022 May;8(5):404-415. doi: 10.1016/j.trecan.2022.01.008. Epub 2022 Feb 3.

DOI:10.1016/j.trecan.2022.01.008
PMID:35125331
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9035058/
Abstract

The host immune response is a potent defense mechanism against cancer development and progression. To survive, cancer cells must develop mechanisms to evade the immune response. Based on this knowledge, a series of new therapies collectively referred to as immunotherapies have been developed and translated to the clinic for treating cancer patients. Although some cancer subtypes have shown strong clinical responses, including curative outcomes in some patients, immunotherapies have not worked as desired for some subtypes and forms of cancers. We provide an overview of the transcriptional mechanisms that drive the response and resistance to immunotherapies. We also discuss possible interventions to enhance the outcomes of immunotherapies by targeting dysregulated transcriptional networks in cancer cells.

摘要

宿主免疫反应是对抗癌症发生和发展的强大防御机制。为了生存,癌细胞必须发展逃避免疫反应的机制。基于这一知识,一系列新的治疗方法被统称为免疫疗法,并已转化为临床,用于治疗癌症患者。尽管一些癌症亚型显示出强烈的临床反应,包括一些患者的治愈结果,但免疫疗法对一些亚型和形式的癌症并没有达到预期的效果。我们提供了一个概述,介绍了驱动免疫疗法反应和抵抗的转录机制。我们还讨论了通过靶向癌细胞中失调的转录网络来增强免疫疗法结果的可能干预措施。

相似文献

1
Transcriptional determinants of cancer immunotherapy response and resistance.癌症免疫疗法反应和抵抗的转录决定因素。
Trends Cancer. 2022 May;8(5):404-415. doi: 10.1016/j.trecan.2022.01.008. Epub 2022 Feb 3.
2
Recent Advances of RNA mA Modifications in Cancer Immunoediting and Immunotherapy.RNA mA 修饰在癌症免疫编辑和免疫治疗中的最新进展。
Cancer Treat Res. 2023;190:49-94. doi: 10.1007/978-3-031-45654-1_3.
3
Understanding and overcoming resistance to immunotherapy in genitourinary cancers.了解并克服泌尿生殖系统癌症的免疫治疗抵抗。
Cancer Biol Ther. 2024 Dec 31;25(1):2342599. doi: 10.1080/15384047.2024.2342599. Epub 2024 Apr 17.
4
Noncoding RNAs as an emerging resistance mechanism to immunotherapies in cancer: basic evidence and therapeutic implications.非编码 RNA 作为癌症免疫治疗的新兴耐药机制:基础证据与治疗意义。
Front Immunol. 2023 Sep 12;14:1268745. doi: 10.3389/fimmu.2023.1268745. eCollection 2023.
5
Natural Killer Cells: The Linchpin for Successful Cancer Immunotherapy.自然杀伤细胞:癌症免疫治疗成功的关键。
Front Immunol. 2021 Apr 28;12:679117. doi: 10.3389/fimmu.2021.679117. eCollection 2021.
6
Epigenetic regulation of tumor immunity.肿瘤免疫的表观遗传调控。
J Clin Invest. 2024 Jun 17;134(12):e178540. doi: 10.1172/JCI178540.
7
Epigenetic regulation in the tumor microenvironment: molecular mechanisms and therapeutic targets.肿瘤微环境中的表观遗传调控:分子机制和治疗靶点。
Signal Transduct Target Ther. 2023 May 22;8(1):210. doi: 10.1038/s41392-023-01480-x.
8
Self-Assembly as a Molecular Strategy to Improve Immunotherapy.自组装作为一种提高免疫疗法的分子策略。
Acc Chem Res. 2020 Nov 17;53(11):2534-2545. doi: 10.1021/acs.accounts.0c00438. Epub 2020 Oct 19.
9
Epigenetic Strategies to Boost Cancer Immunotherapies.增强癌症免疫疗法的表观遗传学策略
Int J Mol Sci. 2017 May 23;18(6):1108. doi: 10.3390/ijms18061108.
10
Genomic determinants of cancer immunotherapy.癌症免疫疗法的基因组决定因素。
Curr Opin Immunol. 2016 Aug;41:32-38. doi: 10.1016/j.coi.2016.05.010. Epub 2016 May 30.

引用本文的文献

1
NSD proteins in anti-tumor immunity and their therapeutic targeting by protein degraders.NSD蛋白在抗肿瘤免疫中的作用及其通过蛋白降解剂进行的治疗靶向
Cell Mol Life Sci. 2025 Jun 30;82(1):268. doi: 10.1007/s00018-025-05806-6.
2
Comprehensive single-cell pan-cancer atlas unveils IFI30+ macrophages as key modulators of intra-tumoral immune dynamics.综合性单细胞泛癌图谱揭示IFI30+巨噬细胞是肿瘤内免疫动力学的关键调节因子。
Front Immunol. 2025 Jan 24;16:1523854. doi: 10.3389/fimmu.2025.1523854. eCollection 2025.
3
Effects of super-enhancers in cancer metastasis: mechanisms and therapeutic targets.超级增强子在癌症转移中的作用:机制和治疗靶点。
Mol Cancer. 2024 Jun 7;23(1):122. doi: 10.1186/s12943-024-02033-8.
4
Tissue-specific thresholds of mutation burden associated with anti-PD-1/L1 therapy benefit and prognosis in microsatellite-stable cancers.与抗 PD-1/L1 治疗获益和预后相关的微卫星稳定型癌症的组织特异性突变负担阈值。
Nat Cancer. 2024 Jul;5(7):1121-1129. doi: 10.1038/s43018-024-00752-x. Epub 2024 Mar 25.
5
Protein tyrosine phosphatases as emerging targets for cancer immunotherapy.蛋白酪氨酸磷酸酶作为癌症免疫治疗的新兴靶点。
Br J Pharmacol. 2023 Dec 20. doi: 10.1111/bph.16304.
6
Pan-cancer analysis and experimental validation revealed the m6A methyltransferase KIAA1429 as a potential biomarker for diagnosis, prognosis, and immunotherapy.泛癌症分析和实验验证揭示了 m6A 甲基转移酶 KIAA1429 作为一种潜在的诊断、预后和免疫治疗的生物标志物。
Aging (Albany NY). 2023 Aug 21;15(17):8664-8691. doi: 10.18632/aging.204968.
7
Probing the Potential of Defense Response-Associated Genes for Predicting the Progression, Prognosis, and Immune Microenvironment of Osteosarcoma.探究防御反应相关基因在预测骨肉瘤进展、预后及免疫微环境方面的潜力
Cancers (Basel). 2023 Apr 21;15(8):2405. doi: 10.3390/cancers15082405.
8
Glioma-derived CCL2 and CCL7 mediate migration of immune suppressive CCR2/CX3CR1 M-MDSCs into the tumor microenvironment in a redundant manner.胶质母细胞瘤衍生的 CCL2 和 CCL7 以冗余方式介导免疫抑制性 CCR2/CX3CR1 M-MDSC 向肿瘤微环境迁移。
Front Immunol. 2023 Jan 4;13:993444. doi: 10.3389/fimmu.2022.993444. eCollection 2022.
9
Design of new drugs for medullary thyroid carcinoma.甲状腺髓样癌新药的设计
Front Oncol. 2022 Dec 5;12:993725. doi: 10.3389/fonc.2022.993725. eCollection 2022.
10
The Crossroads of Cancer Epigenetics and Immune Checkpoint Therapy.癌症表观遗传学与免疫检查点治疗的交汇点。
Clin Cancer Res. 2023 Apr 3;29(7):1173-1182. doi: 10.1158/1078-0432.CCR-22-0784.

本文引用的文献

1
Engineering enhanced CAR T-cells for improved cancer therapy.工程改造增强型嵌合抗原受体T细胞以改善癌症治疗。
Nat Cancer. 2021 Aug;2(8):780-793. doi: 10.1038/s43018-021-00241-5. Epub 2021 Aug 19.
2
The PEMDAC phase 2 study of pembrolizumab and entinostat in patients with metastatic uveal melanoma.派姆单抗和恩替诺特联合治疗转移性葡萄膜黑色素瘤患者的 PEMDAC 二期研究。
Nat Commun. 2021 Aug 27;12(1):5155. doi: 10.1038/s41467-021-25332-w.
3
Tumor-infiltrating lymphocyte treatment for anti-PD-1-resistant metastatic lung cancer: a phase 1 trial.肿瘤浸润淋巴细胞治疗抗 PD-1 耐药性转移性肺癌:一项 1 期试验。
Nat Med. 2021 Aug;27(8):1410-1418. doi: 10.1038/s41591-021-01462-y. Epub 2021 Aug 12.
4
EZH2 inhibits NK cell-mediated antitumor immunity by suppressing CXCL10 expression in an HDAC10-dependent manner.EZH2 通过依赖于 HDAC10 的方式抑制 CXCL10 的表达,从而抑制 NK 细胞介导的抗肿瘤免疫。
Proc Natl Acad Sci U S A. 2021 Jul 27;118(30). doi: 10.1073/pnas.2102718118.
5
DNA methylation-based prediction of response to immune checkpoint inhibition in metastatic melanoma.基于 DNA 甲基化的预测转移性黑色素瘤对免疫检查点抑制的反应。
J Immunother Cancer. 2021 Jul;9(7). doi: 10.1136/jitc-2020-002226.
6
Combining CD47 blockade with trastuzumab eliminates HER2-positive breast cancer cells and overcomes trastuzumab tolerance.阻断 CD47 与曲妥珠单抗联用可消除 HER2 阳性乳腺癌细胞并克服曲妥珠单抗耐受。
Proc Natl Acad Sci U S A. 2021 Jul 20;118(29). doi: 10.1073/pnas.2026849118.
7
Engineered TCR-T Cell Immunotherapy in Anticancer Precision Medicine: Pros and Cons.工程化 TCR-T 细胞免疫疗法在抗肿瘤精准医学中的利与弊。
Front Immunol. 2021 Mar 30;12:658753. doi: 10.3389/fimmu.2021.658753. eCollection 2021.
8
Systemic immunity in cancer.癌症的系统性免疫。
Nat Rev Cancer. 2021 Jun;21(6):345-359. doi: 10.1038/s41568-021-00347-z. Epub 2021 Apr 9.
9
The Next Decade of Immune Checkpoint Therapy.免疫检查点治疗的下一个十年。
Cancer Discov. 2021 Apr;11(4):838-857. doi: 10.1158/2159-8290.CD-20-1680.
10
FDA approves fourth CAR-T cell therapy.美国食品药品监督管理局批准第四种嵌合抗原受体T细胞疗法。
Nat Rev Drug Discov. 2021 Mar;20(3):166. doi: 10.1038/d41573-021-00031-9.