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中华乳腺病杂志(电子版) ›› 2026, Vol. 20 ›› Issue (03) : 179 -183. doi: 10.3877/cma.j.issn.1674-0807.2026.03.008

综述

系统性红斑狼疮与乳腺癌关系的研究进展
黄家骏1,2, 周奕延1,2, 王斐然1, 何志贤1,()   
  1. 1 226001 南通,南通大学附属医院甲乳外科
    2 226001 南通,南通大学医学院
  • 收稿日期:2025-12-08 出版日期:2026-06-01
  • 通信作者: 何志贤

Research progress on the relationship between systemic lupus erythematosus and breast cancer

Jiajun Huang, Yiyan Zhou, Feiran Wang   

  • Received:2025-12-08 Published:2026-06-01
引用本文:

黄家骏, 周奕延, 王斐然, 何志贤. 系统性红斑狼疮与乳腺癌关系的研究进展[J/OL]. 中华乳腺病杂志(电子版), 2026, 20(03): 179-183.

Jiajun Huang, Yiyan Zhou, Feiran Wang. Research progress on the relationship between systemic lupus erythematosus and breast cancer[J/OL]. Chinese Journal of Breast Disease(Electronic Edition), 2026, 20(03): 179-183.

系统性红斑狼疮(SLE)与乳腺癌发生风险及共病结局的关系长期存在争议。现有证据在研究设计、人群特征及效应量指标等方面存在较大异质性,导致临床上对两者关系的认识尚不一致。近年来,流行病学、遗传学及基础实验研究提示,SLE患者乳腺癌总体发病风险并未明显升高,且部分人群可观察到风险降低趋势,但该趋势在不同种族和地区中存在差异。其潜在机制可能涉及免疫监视增强、DNA损伤修复干预、激素暴露减少以及部分SLE治疗药物的抗肿瘤相关作用。与此同时,乳腺癌治疗药物也可能影响SLE的发生及预后。本文围绕SLE患者发生乳腺癌的流行病学特征、SLE可能抑制乳腺癌的潜在机制以及两者的交互作用进行总结,以期为相关人群的风险评估和临床管理提供参考。

表1 SLE与乳腺癌关系的核心临床与流行病学研究
表2 SLE抑制乳腺癌发生的主要分子机制研究
研究者 研究类型 研究对象 主要机制
Ding等36 生物信息学分析 SLE、乳腺癌 膜金属内肽酶
Hoxhaj等37 综述 癌症代谢重编程 PI3K-AKT信号网络
Lim等38 基础实验研究 癌症 (BRCA2突变相关) BRCA2、同源定向修复
Jimenez-Sainz等39 基础实验研究 癌症 (BRCA2变异相关) BRCA2 BRC错义突变 (S1221P、T1980I、T1346I)
Hansen等40 基础实验研究 BRCA2缺陷型肿瘤 (乳腺癌/卵巢癌/脑胶质瘤) 狼疮自身抗体3E10,DNA修复(HDR/BER)
Noble等41 基础实验研究 BRCA2缺陷型结肠癌 溶核性狼疮自身抗体 5C6
Al-Shami等42 综述 乳腺癌 雌激素及代谢产物,ER
Van Eaton等43 药代/药效动力学基础研究 乳腺癌 (2D/3D模型及异种移植模型) 自噬依赖性(羟氯喹)
Amaravadi44 评论 卵巢癌 ARHI诱导的自噬,肿瘤休眠
Yang等45 基础实验研究 ER阳性乳腺癌 PI3K、自噬(氯喹)、Bim/PUMA
Cocco等46 综述 乳腺癌 自噬(氯喹/羟氯喹)
Amaravadi等47 综述 癌症 (一般性) 自噬调控,溶酶体
Cuzick等48 随机对照临床试验 (IBIS-Ⅱ) 乳腺癌高风险人群 芳香化酶(阿那曲唑),乳腺癌预防
Thorén等49 临床队列研究 乳腺癌 CYP2D6酶(他莫昔芬),乳房X线密度
Liu等50 基础实验研究 乳腺癌 (人乳腺上皮及乳腺癌细胞模型) PIK3CA H1047R突变,膜金属内肽酶,细胞衰老,巨噬细胞极化
Rahim等51 基础实验研究 乳腺癌 (细胞模型) 促细胞分化(氯喹、羟氯喹、全反式维甲酸), 组蛋白乙酰化(羟氯喹、全反式维甲酸)
Valdes-Abadia等52 基础实验研究 乳腺癌 (MDA-MB-231细胞系) Kv10.1通道(氯喹),细胞迁移
图1 系统性红斑狼疮与乳腺癌的双向交互作用及潜在机制 注:SLE可能通过基因及信号通路调控、免疫监视增强、激素暴露减少及治疗药物作用等途径影响乳腺癌发生风险;乳腺癌治疗也可能通过内分泌调节等机制影响SLE的发生或疾病活动。SLE为系统性红斑狼疮;MME为膜金属内肽酶;PI3K/AKT为磷脂酰肌醇3-激酶/蛋白激酶B信号通路;FOXO为叉头框O转录因子;BRCA1/2为乳腺癌易感基因1/2;SERM为选择性雌激素受体调节剂;ER-α为雌激素受体α;Kv10.1为电压门控钾通道10.1;TP53为肿瘤蛋白p53
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