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A novel extracellular vesicle-engineered immunotherapy drug for Her2 breast cancer.

1/5 보강
Journal of advanced research 📖 저널 OA 68.2% 2024: 1/1 OA 2025: 33/56 OA 2026: 56/75 OA 2024~2026 2026
Retraction 확인
출처

Lu X, Yuan W, Zeng X, Zhang F, Zhang C, Li X, Guo J, Hao J, Zhang G, Wang J, Wu H, Cai Z

📝 환자 설명용 한 줄

Trastuzumab profoundly improves outcomes of Her2 breast cancer (BC) patients, but eventual drug resistance is inevitable.

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↓ .bib ↓ .ris
APA Lu X, Yuan W, et al. (2026). A novel extracellular vesicle-engineered immunotherapy drug for Her2 breast cancer.. Journal of advanced research. https://doi.org/10.1016/j.jare.2026.01.067
MLA Lu X, et al.. "A novel extracellular vesicle-engineered immunotherapy drug for Her2 breast cancer.." Journal of advanced research, 2026.
PMID 41592682 ↗

Abstract

Trastuzumab profoundly improves outcomes of Her2 breast cancer (BC) patients, but eventual drug resistance is inevitable. Therefore, new treatment options are urgently needed. Here, we modify extracellular vesicles (EVs) with a Her2 single-chain variable fragment of trastuzumab (EVs/Her2-scFv) to target Her2 BC and found that EVs/Her2-scFv inhibit human Her2 orthotopic BC comparable to trastuzumab and also uniquely suppress brain metastasies. Moreover, EVs/Her2-scFv loaded with rabeprazole (EVs/Her2-scFv/Rabe) effectively improve tumor immunosuppressive microenvironment and abnormal vasculature of Her2 BC by reducing tumor EVs. When further anchored with CD8 T cell chemotactic CXCL9, CXCL9-loaded EVs/Her2-scFv/Rabe (EVs/Her2-scFv/CXCL9/Rabe) facilitate CD8 T cell recruitment and subsequent activation, thereby exhibiting immunotherapeutic effects on mouse Her2 BC. In BC patient-derived tumor organoids (PDOs) and peripheral blood mononuclear cell coculture systems, EVs/Her2-scFv/CXCL9/Rabe limit PDO growth by blocking Her2 signaling and activating CD8 T cells. Besides, EVs/Her2-scFv/CXCL9/Rabe are low-immunogenic with biosafety. Altogether, EVs/Her2-scFv/CXCL9/Rabe hold high potential in Her2 BC therapy.

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