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三阴性乳腺癌抗雄激素治疗的现状与进展

Current Status and Advances in Anti-Androgen Therapy for Triple-Negative Breast Cancer.

作者信息

Li Jing-Bo, Xia Wen-Fei

机构信息

The Second Clinical Medical School of Shandong University, Jinan, 250033, China.

Department of Breast and Thyroid Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.

出版信息

Curr Med Sci. 2025 Aug 25. doi: 10.1007/s11596-025-00094-4.

DOI:10.1007/s11596-025-00094-4
PMID:40853613
Abstract

The heterogeneity of triple-negative breast cancer (TNBC) has spurred the exploration of precision therapies based on molecular subtypes, with the androgen receptor (AR)-positive subtype emerging as a potential therapeutic target. The treatment of AR-positive TNBC relies primarily on androgen receptor antagonists, such as enobosarm, bicalutamide, and enzalutamide. To enhance efficacy, researchers are investigating combination therapies that integrate anti-androgen agents with chemotherapy, immunotherapy, or PARP inhibitors. Additionally, studies have revealed that the AR signaling pathway regulates the tumor microenvironment, and AR inhibition may potentiate the efficacy of immune checkpoint inhibitors. However, anti-AR therapies face significant limitations and challenges due to multifaceted factors, necessitating further resolution. With continued advancements, AR-targeted therapy holds promise as a critical component of personalized treatment strategies for TNBC.

摘要

三阴性乳腺癌(TNBC)的异质性推动了基于分子亚型的精准治疗探索,雄激素受体(AR)阳性亚型成为一个潜在的治疗靶点。AR阳性TNBC的治疗主要依赖于雄激素受体拮抗剂,如恩杂鲁胺、比卡鲁胺和恩扎卢胺。为提高疗效,研究人员正在研究将抗雄激素药物与化疗、免疫治疗或PARP抑制剂相结合的联合疗法。此外,研究表明AR信号通路调节肿瘤微环境,抑制AR可能增强免疫检查点抑制剂的疗效。然而,由于多方面因素,抗AR治疗面临重大局限和挑战,需要进一步解决。随着不断进步,AR靶向治疗有望成为TNBC个性化治疗策略的关键组成部分。

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本文引用的文献

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Molecular classification of hormone receptor-positive /HER2-positive breast cancer reveals potential neoadjuvant therapeutic strategies.激素受体阳性/人表皮生长因子受体2阳性乳腺癌的分子分类揭示了潜在的新辅助治疗策略。
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NONO interacts with nuclear PKM2 and directs histone H3 phosphorylation to promote triple-negative breast cancer metastasis.
NONO与细胞核内的丙酮酸激酶M2相互作用,并引导组蛋白H3磷酸化以促进三阴性乳腺癌转移。
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