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克服膀胱癌免疫逃逸的策略。

Strategies for Overcoming Immune Evasion in Bladder Cancer.

机构信息

Department of Health Sciences, The Graduate School of Dong-A University, Busan 49315, Republic of Korea.

Department of Korean Medicine, College of Korean Medicine, Woosuk University, Jeonju 54986, Republic of Korea.

出版信息

Int J Mol Sci. 2024 Mar 7;25(6):3105. doi: 10.3390/ijms25063105.


DOI:10.3390/ijms25063105
PMID:38542078
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10970137/
Abstract

Tumors intricately shape a highly immunosuppressive microenvironment, hampering effective antitumor immune responses through diverse mechanisms. Consequently, achieving optimal efficacy in cancer immunotherapy necessitates the reorganization of the tumor microenvironment and restoration of immune responses. Bladder cancer, ranking as the second most prevalent malignant tumor of the urinary tract, presents a formidable challenge. Immunotherapeutic interventions including intravesical BCG and immune checkpoint inhibitors such as atezolizumab, avelumab, and pembrolizumab have been implemented. However, a substantial unmet need persists as a majority of bladder cancer patients across all stages do not respond adequately to immunotherapy. Bladder cancer establishes a microenvironment that can actively hinder an efficient anti-tumor immune response. A deeper understanding of immune evasion mechanisms in bladder cancer will aid in suppressing recurrence and identifying viable therapeutic targets. This review seeks to elucidate mechanisms of immune evasion specific to bladder cancer and explore novel pathways and molecular targets that might circumvent resistance to immunotherapy.

摘要

肿瘤错综复杂地塑造了高度免疫抑制的微环境,通过多种机制阻碍有效的抗肿瘤免疫反应。因此,要在癌症免疫治疗中实现最佳疗效,就需要重新组织肿瘤微环境并恢复免疫反应。膀胱癌是泌尿系统第二大常见恶性肿瘤,极具挑战性。已经实施了包括膀胱内卡介苗在内的免疫治疗干预措施,以及免疫检查点抑制剂,如阿替利珠单抗、avelumab 和 pembrolizumab。然而,仍然存在很大的未满足需求,因为大多数膀胱癌患者在所有阶段都不能对免疫治疗有足够的反应。膀胱癌建立了一个可以积极阻碍有效抗肿瘤免疫反应的微环境。深入了解膀胱癌中的免疫逃逸机制将有助于抑制复发和确定可行的治疗靶点。本综述旨在阐明膀胱癌特有的免疫逃逸机制,并探讨可能规避免疫治疗耐药性的新途径和分子靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0765/10970137/672d199c8fd3/ijms-25-03105-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0765/10970137/a5803f58850c/ijms-25-03105-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0765/10970137/672d199c8fd3/ijms-25-03105-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0765/10970137/a5803f58850c/ijms-25-03105-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0765/10970137/672d199c8fd3/ijms-25-03105-g002.jpg

相似文献

[1]
Strategies for Overcoming Immune Evasion in Bladder Cancer.

Int J Mol Sci. 2024-3-7

[2]
Mechanisms of immune evasion in bladder cancer.

Cancer Immunol Immunother. 2019-12-6

[3]
Bladder cancer, a unique model to understand cancer immunity and develop immunotherapy approaches.

J Pathol. 2019-6-24

[4]
Systemic Immunotherapy of Non-Muscle Invasive Mouse Bladder Cancer with Avelumab, an Anti-PD-L1 Immune Checkpoint Inhibitor.

Cancer Immunol Res. 2016-2-26

[5]
BCG therapy downregulates HLA-I on malignant cells to subvert antitumor immune responses in bladder cancer.

J Clin Invest. 2022-6-15

[6]
Immune regulation and the tumor microenvironment in anti-PD-1/PDL-1 and anti-CTLA-4 therapies for cancer immune evasion: A bibliometric analysis.

Hum Vaccin Immunother. 2024-12-31

[7]
Checkpoint inhibitors in BCG-unresponsive nonmuscle invasive bladder cancer: can they help spare the bladder?

Immunotherapy. 2021-9

[8]
Rationale and Outcomes for Neoadjuvant Immunotherapy in Urothelial Carcinoma of the Bladder.

Eur Urol Oncol. 2020-12

[9]
Tumor microenvironment-mediated immune evasion in hepatocellular carcinoma.

Front Immunol. 2023

[10]
The Tumor Microenvironment of Bladder Cancer.

Adv Exp Med Biol. 2020

引用本文的文献

[1]
HDL cholesterol esters mediate the genetic link between sedentary behavior and urological cancers: Insights from mediation and validation analyses.

Medicine (Baltimore). 2025-5-2

本文引用的文献

[1]
Novel immunotherapeutic options for BCG-unresponsive high-risk non-muscle-invasive bladder cancer.

Cancer Med. 2023-12

[2]
Cancer-associated fibroblasts-derived CXCL12 enhances immune escape of bladder cancer through inhibiting P62-mediated autophagic degradation of PDL1.

J Exp Clin Cancer Res. 2023-11-25

[3]
FAM171B stabilizes vimentin and enhances CCL2-mediated TAM infiltration to promote bladder cancer progression.

J Exp Clin Cancer Res. 2023-11-2

[4]
Toll-like receptor-guided therapeutic intervention of human cancers: molecular and immunological perspectives.

Front Immunol. 2023

[5]
Cancer-Associated Fibroblast-Induced Remodeling of Tumor Microenvironment in Recurrent Bladder Cancer.

Adv Sci (Weinh). 2023-11

[6]
BCG-Unresponsive Non-Muscle-Invasive Bladder Cancer: Current Treatment Landscape and Novel Emerging Molecular Targets.

Int J Mol Sci. 2023-8-9

[7]
Tumor-derived prostaglandin E2 programs cDC1 dysfunction to impair intratumoral orchestration of anti-cancer T cell responses.

Immunity. 2023-6-13

[8]
Complementary roles of EP2 and EP4 receptors in malignant glioma.

Br J Pharmacol. 2023-10

[9]
HLA-G expression in transitional bladder carcinoma. Relationship with tumor invasion level and patient survival: Experience in a public hospital in Argentina.

Hum Immunol. 2023-8

[10]
T cell subsets, regulatory T, regulatory B cells and proinflammatory cytokine profile in Schistosoma haematobium associated bladder cancer: First report from Upper Egypt.

PLoS Negl Trop Dis. 2023-4

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