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作 者:Huiqin Chen Guanqun Guo Gen Yang 陈慧芹;郭冠群;杨根
机构地区:[1]Wenzhou Institute,University of Chinese Academy of Sciences,Wenzhou 325000,China [2]School of Physics,Peking University,Beijing 100871,China
出 处:《Science Bulletin》2024年第17期2653-2655,共3页科学通报(英文版)
基 金:National Natural Science Foundation of China (12375334);Key Program of Wenzhou Institute, University of Chinese Academy of Sciences (WIUCASQD2021015)。
摘 要:In recent years, immune checkpoint blockade (ICB) therapy,represented by molecules such as programmed cell death 1 (PD-1), programmed death ligand 1 (PD-L1), and cytotoxic T-lymphocyte-associated protein 4 (CTLA-4), has made revolutionary progress in the field of tumor treatment. However, the efficacy of ICB in different clinical cancer patients varies greatly, with most patients showing little or no response to the treatments [1]. The suppressive tumor immune microenvironment (TME) containing high myeloid cells is a major cause of the failure of immunotherapy[2,3].
关 键 词:PATIENTS IMMUNOTHERAPY CD30
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