Mesenchymal stromal cell therapy for pancreatic ductal adenocarcinoma: mechanisms, applications, and challenges
DOI：10.3872/j.issn.1007-385X.2026.06.001
- VernacularTitle:间充质基质细胞疗法用于胰腺导管腺癌治疗的机制、应用及挑战
- Author:
DONG Yuhui1,2
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LI Yu2,3,4
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GAO Jie2,3,5
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LI Zh aoshen2,3,5,6
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Author Information
1. School of Health Science and Engineering, University of Shanghai for Science and Technology, Shanghai 200093, China;
2. Changhai Clinical Research Center, Changhai Hospital of Naval Medical University, Shanghai 200433, China;
3. Department of Gastroenterology, National Clinical Research Center for Digestive Diseases, Changhai Hospital of Naval Medical University, Shanghai 200433, China;
4. Translational Medical Research Center, Naval Medical University, Shanghai 200433, China;
5. Shanghai Key Laboratory of Nautical Medicine and Translation of Drugs and Medical Devices, Shanghai 200433, China;
6. National Key Laboratory of Immunology and Inflammation, Naval Medical University, Shanghai 200433, China
- Publication Type:Journal Article
- Keywords:
胰腺导管腺癌；肿瘤微环境；肿瘤归巢；间充质基质细胞；工程化间充质基质细胞；药物递送
- From:
Chinese Journal of Cancer Biotherapy
2026;33(6):589-601
- CountryChina
- Language:Chinese
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Abstract:
胰腺导管腺癌（pancreatic ductal adenocarcinoma, PDAC）具有高度侵袭性、早期诊断率低且对全身治疗总体反应有限，其致密纤维化基质、异常血管与免疫抑制性肿瘤微环境共同导致药物渗透不足与免疫“冷肿瘤”特征，是疗效受限的重要原因。间充质基质细胞（mesenchymal stromal cell, MSC）具有趋炎性迁移、免疫调控与旁分泌效应，可作为“活体递送载体”将细胞因子、化疗药物、溶瘤病毒及自杀基因等定向输送至肿瘤区域，从而为突破基质屏障与重塑微环境提供策略空间（摘要图）。然而，MSC在肿瘤情境下存在显著可塑性与“双刃剑效应”，可能被肿瘤微环境再教育而表现出免疫抑制、促血管生成、促纤维化、促侵袭及促耐药等不良作用；同时其体内分布与载荷释放缺乏可量化与可控证据链，制备工艺与功能质控标准不统一，构成转化瓶颈。本文重点评述MSC与PDAC微环境相互作用机制及工程化MSC递送治疗性蛋白、药物、溶瘤病毒与自杀基因等研究进展，并探讨安全性、有效性评价与质量控制挑战。发展具有微环境响应释放与安全开关的可编程MSC平台，建立面向肿瘤治疗的功能评价或放行体系，并推进MSC衍生细胞外囊泡等无细胞策略，或将更有利于提升可重复性与降低体内持久性相关风险。
- Full text:2026070710215385447202606001.pdf
