尿激酶受体
癌症研究
T细胞
受体
纤溶酶原激活剂
细胞培养
细胞
中枢神经系统
生物
体外
嵌合抗原受体
抗原
细胞毒性T细胞
免疫学
T细胞受体
胶质瘤
肿瘤进展
医学
下调和上调
激活剂(遗传学)
化学
作者
William T. Maich,Muhammad Vaseem Shaikh,Anish Puri,Martin A. Rossotti,Shan Grewal,Aapti Khanna,Alisha Anand,Nicholas Mikolajewicz,Mathieu P. Seyfrid,Dillon A. McKenna,Minomi Subapanditha,Daniel Mobilio,Greg Hussack,Joey Sheff,J. Hill,Mo Taleb,Jacek M. Kwiecień,Sabra Salim,Neil Savage,Bill Wang
标识
DOI:10.1126/scitranslmed.aea8381
摘要
Glioblastoma (GBM) comprises nearly 15% of primary central nervous system (CNS) tumors and 50% of malignant primary CNS tumors worldwide. Considerable tumoral heterogeneity exists in GBM, leading to inefficacy of current treatments and the absence of meaningful improvements in frontline therapies in the past 20 years. Through multiomic analysis of patient-derived primary and recurrent GBM cell lines, we identified the urokinase plasminogen activator receptor (uPAR) as a protumorigenic marker of putative brain tumor-initiating cells and a potential therapeutic target. We found that genetic disruption of uPAR expression impaired protumorigenic characteristics in vitro and in vivo, highlighting its biological role in tumorigenesis. We then generated uPAR-specific chimeric antigen receptor (CAR) T cells, which demonstrated potent antitumor activity in recurrent GBM patient-derived xenograft models. In addition to direct tumor cell killing, we found that uPAR is expressed on GBM-associated macrophages, enabling uPAR CAR T cells to target both GBM itself and cells in the tumor microenvironment. Together, these data illustrate the potency and therapeutic potential of targeting uPAR in GBM.
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