下一代肿瘤不可知靶点即将出现
Next-generation tumor-agnostic targets on the horizon.
肿瘤不可知药物开发将肿瘤学重新聚焦于共享的分子依赖性而非组织来源，从而能够针对跨肿瘤的罕见可操作驱动因素进行高效开发。
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CELL INTELLIGENCE · 肿瘤细胞治疗研究
肿瘤细胞治疗研究
HR(+) 乳腺癌对 CDK4/6 抑制剂耐药的免疫学机制
英文原题：An immunological mechanism of resistance to CDK4/6 inhibitors in HR(+) breast cancer.
查看英文原题
An immunological mechanism of resistance to CDK4/6 inhibitors in HR(+) breast cancer.
研究概要
CDK4/6 抑制剂是 HR + HER2 - 乳腺癌临床管理的核心。
中文摘要
CDK4/6 抑制剂是 HR+HER2- 乳腺癌临床管理的核心。我们最近证明，CDK4/6 抑制后通过 CCL2 依赖性机制被招募到肿瘤微环境的免疫抑制性、分泌 IL17 的 γδ T 细胞，可将肿瘤相关巨噬细胞重极化为与治疗耐药相关的 CX3CR1+ 表型。
展开英文摘要原文
CDK4/6 inhibitors are central to the clinical management of HR + HER2 - breast cancer. We have recently demonstrated that immunosuppressive, IL17-secreting γδ T cells recruited to the tumor microenvironment by a CCL2-dependent mechanism upon CDK4/6 inhibition can repolarize tumor-associated macrophages toward a CX3CR1 + phenotype associated with resistance to therapy.
论文信息
- 作者
- Galassi C、Petroni G、Knott SRV、Galluzzi L
- 第一作者单位
- Department of Pharmacology, Weill Cornell Medical College, New York, NY, USA.United States
- 通讯作者单位
- Cancer Signaling and Microenvironment Program, Fox Chase Cancer Center, Philadelphia, PA, USA.United States
- 文献类型
- 社论 · 美国政府（非公共卫生署）资助研究 · 美国 NIH 资助研究
- 期刊
- Oncoimmunology2025 Dec
- 原文标识
- PubMed 40662849 · DOI 10.1080/2162402X.2025.2520269