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肿瘤细胞中 GPR65 失活通过巨噬细胞重塑驱动抗原非依赖性 CAR-T 细胞耐药

英文原题:GPR65 Inactivation in Tumor Cells Drives Antigen-Independent CAR T-cell Resistance via Macrophage Remodeling.

查看英文原题

GPR65 Inactivation in Tumor Cells Drives Antigen-Independent CAR T-cell Resistance via Macrophage Remodeling.

PubMed 2025/05/02(内容时间) Cancer Discov Q1 · IF 29.5(JCR 2025)

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中文摘要

该研究将 GPR65 确定为 B 细胞急性淋巴细胞白血病对 CAR-T 细胞治疗反应的重要决定因素。值得注意的是,GPR65 缺失提示 CAR-T 耐药。通过强调靶向 VEGFA 或宿主巨噬细胞的治疗潜力,我们的研究确定了通过肿瘤微环境调控来优化 CAR-T 细胞治疗在血液系统恶性肿瘤中结局的途径。

展开英文摘要原文

The study identifies GPR65 as an important determinant of B-cell acute lymphoblastic leukemia response to CAR T-cell therapy. Notably, GPR65 absence signals CAR T resistance. By emphasizing the therapeutic potential of targeting VEGFA or host macrophages, our study identifies routes to optimize CAR T-cell therapy outcomes in hematologic malignancies via tumor microenvironment manipulation.

论文信息

作者
Mavuluri J、Dhungana Y、Jones LL、Bhatara S、Shi H、Yang X、Lim SE、Reyes N
单位
Department of Pathology, St. Jude Children's Research Hospital, Memphis, Tennessee.
期刊
Cancer discovery2025 May 2
原文标识
PubMed 39998425 · DOI 10.1158/2159-8290.CD-24-0841