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三阴性乳腺癌免疫治疗的当前进展与挑战

Current Progresses and Challenges of Immunotherapy in Triple-Negative Breast Cancer.

作者信息

Mediratta Karan, El-Sahli Sara, D'Costa Vanessa, Wang Lisheng

机构信息

Department of Biochemistry, Microbiology and Immunology, Faculty of Medicine, University of Ottawa, 451 Smyth Road, Ottawa, ON K1H 8M5, Canada.

Centre for Infection, Immunity and Inflammation, University of Ottawa, 451 Smyth Road, Ottawa, ON K1H 8M5, Canada.

出版信息

Cancers (Basel). 2020 Nov 26;12(12):3529. doi: 10.3390/cancers12123529.


DOI:10.3390/cancers12123529
PMID:33256070
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7761500/
Abstract

With improved understanding of the immunogenicity of triple-negative breast cancer (TNBC), immunotherapy has emerged as a promising candidate to treat this lethal disease owing to the lack of specific targets and effective treatments. While immune checkpoint inhibition (ICI) has been effectively used in immunotherapy for several types of solid tumor, monotherapies targeting programmed death 1 (PD-1), its ligand PD-L1, or cytotoxic T lymphocyte-associated protein 4 (CTLA-4) have shown little efficacy for TNBC patients. Over the past few years, various therapeutic candidates have been reviewed, attempting to improve ICI efficacy on TNBC through combinatorial treatment. In this review, we describe the clinical limitations of ICI and illustrate candidates from an immunological, pharmacological, and metabolic perspective that may potentiate therapy to improve the outcomes of TNBC patients.

摘要

随着对三阴性乳腺癌(TNBC)免疫原性的认识不断提高,由于缺乏特异性靶点和有效治疗方法,免疫疗法已成为治疗这种致命疾病的一种有前景的选择。虽然免疫检查点抑制(ICI)已有效应用于多种实体瘤的免疫治疗,但针对程序性死亡蛋白1(PD-1)、其配体PD-L1或细胞毒性T淋巴细胞相关蛋白4(CTLA-4)的单一疗法对TNBC患者疗效甚微。在过去几年中,人们对各种治疗方案进行了评估,试图通过联合治疗提高ICI对TNBC的疗效。在本综述中,我们描述了ICI的临床局限性,并从免疫学、药理学和代谢角度阐述了可能增强治疗效果以改善TNBC患者预后的候选方案。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f1d/7761500/8de08e2d186f/cancers-12-03529-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f1d/7761500/c1c37fa2bd6f/cancers-12-03529-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f1d/7761500/8de08e2d186f/cancers-12-03529-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f1d/7761500/c1c37fa2bd6f/cancers-12-03529-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f1d/7761500/8de08e2d186f/cancers-12-03529-g002.jpg

相似文献

[1]
Current Progresses and Challenges of Immunotherapy in Triple-Negative Breast Cancer.

Cancers (Basel). 2020-11-26

[2]
Progress and challenges of immunotherapy in triple-negative breast cancer.

Biochim Biophys Acta Rev Cancer. 2021-12

[3]
Immune checkpoint inhibitors for triple-negative breast cancer: From immunological mechanisms to clinical evidence.

Int Immunopharmacol. 2021-9

[4]
Inhibition of MYC suppresses programmed cell death ligand-1 expression and enhances immunotherapy in triple-negative breast cancer.

Chin Med J (Engl). 2022-10-20

[5]
Immunotherapy Enhancement by Targeting Extracellular Tumor pH in Triple-Negative Breast Cancer Mouse Model.

Cancers (Basel). 2023-10-11

[6]
Prospects of Immunotherapy for Triple-Negative Breast Cancer.

Front Oncol. 2022-1-17

[7]
Immunotherapy in triple-negative breast cancer.

Med Oncol. 2017-12-18

[8]
Oncolytic adenoviruses synergistically enhance anti-PD-L1 and anti-CTLA-4 immunotherapy by modulating the tumour microenvironment in a 4T1 orthotopic mouse model.

Cancer Gene Ther. 2022-5

[9]
Novel Dual-Mode NIR-II/MRI Nanoprobe Targeting PD-L1 Accurately Evaluates the Efficacy of Immunotherapy for Triple-Negative Breast Cancer.

Int J Nanomedicine. 2023

[10]
Checkpoint inhibitors in triple-negative breast cancer (TNBC): Where to go from here.

Cancer. 2018-2-9

引用本文的文献

[1]
Immunotherapy in breast cancer: current landscape and emerging trends.

Exp Hematol Oncol. 2025-5-22

[2]
Inhibiting glycolysis facilitated checkpoint blockade therapy for triple-negative breast cancer.

Discov Oncol. 2025-4-17

[3]
Tailored therapies for triple-negative breast cancer: current landscape and future perceptions.

Naunyn Schmiedebergs Arch Pharmacol. 2025-3-3

[4]
Classifications of triple-negative breast cancer: insights and current therapeutic approaches.

Cell Biosci. 2025-2-1

[5]
inhibits invasion and metastasis of triple-negative breast cancer cells through multiple targets and pathways.

Nan Fang Yi Ke Da Xue Xue Bao. 2025-1-20

[6]
Unveiling the role of TGF-β signaling pathway in breast cancer prognosis and immunotherapy.

Front Oncol. 2024-11-27

[7]
Biomaterials' enhancement of immunotherapy for breast cancer by targeting functional cells in the tumor micro-environment.

Front Immunol. 2024

[8]
Cytotoxic Autophagy: A Novel Treatment Paradigm against Breast Cancer Using Oleanolic Acid and Ursolic Acid.

Cancers (Basel). 2024-10-1

[9]
Tumor-intrinsic CDC42BPB confers resistance to anti-PD-1 immune checkpoint blockade in breast cancer.

Mol Ther. 2024-10-2

[10]
Targeting cytotoxic lymphocyte antigen 4 (CTLA-4) in breast cancer.

Eur J Med Res. 2024-7-2

本文引用的文献

[1]
Primary results from IMpassion131, a double-blind, placebo-controlled, randomised phase III trial of first-line paclitaxel with or without atezolizumab for unresectable locally advanced/metastatic triple-negative breast cancer.

Ann Oncol. 2021-8

[2]
Targeting the JAK/STAT pathway in solid tumors.

J Cancer Metastasis Treat. 2020

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A Phase I Trial of Talimogene Laherparepvec in Combination with Neoadjuvant Chemotherapy for the Treatment of Nonmetastatic Triple-Negative Breast Cancer.

Clin Cancer Res. 2021-2-15

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USP6NL mediated by LINC00689/miR-142-3p promotes the development of triple-negative breast cancer.

BMC Cancer. 2020-10-14

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A miR-210-3p regulon that controls the Warburg effect by modulating HIF-1α and p53 activity in triple-negative breast cancer.

Cell Death Dis. 2020-9-9

[6]
Why natural killer cells in triple negative breast cancer?

World J Clin Oncol. 2020-7-24

[7]
Immune-Driven Pathogenesis of Neurotoxicity after Exposure of Cancer Patients to Immune Checkpoint Inhibitors.

Int J Mol Sci. 2020-8-11

[8]
Autophagy regulates fatty acid availability for oxidative phosphorylation through mitochondria-endoplasmic reticulum contact sites.

Nat Commun. 2020-8-13

[9]
Autophagy deficiency promotes triple-negative breast cancer resistance to T cell-mediated cytotoxicity by blocking tenascin-C degradation.

Nat Commun. 2020-7-30

[10]
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J Bioenerg Biomembr. 2020-10

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