Harnessing Autologous Immune Effector Mechanisms in Acute Myeloid Leukemia: 2023 Update of Trials and Tribulations

奥佐美星 医学 CD33 嵌合抗原受体 免疫系统 免疫学 髓系白血病 Blinatumoab公司 阿糖胞苷 髓样 免疫疗法 临床试验 白血病 癌症研究 川地34 内科学 生物 CD19 遗传学 干细胞
作者
Shyam A. Patel,Elisa Bello,Andrew F. Wilks,Jonathan M. Gerber,Narayanan Sadagopan,Jan Černý
出处
期刊:Leukemia Research [Elsevier BV]
卷期号:134: 107388-107388
标识
DOI:10.1016/j.leukres.2023.107388
摘要

Numerous recent advances have been made in therapeutic approaches toward acute myeloid leukemia (AML). Since 2017, we have seen eleven novel Food & Drug Administration (FDA)-approved medications for AML, all of which extend beyond the classical cytarabine-based cytostatic chemotherapy. In the recent two decades, the role of immune surveillance in AML has been intensively investigated. The power of one's own innate and adaptive immunity has been harnessed pharmacologically toward the goal of clearance of AML cells. Specifically, pre-clinical studies have shown great promise for antibodies that disinhibit T cells and macrophages by blocking checkpoint receptors within the immunologic synapse, thereby resulting in the elimination of AML cells. Anti-CD33 CAR-T therapies and anti-CD3/CD123 bispecific antibodies have also exhibited encouraging results in pre-clinical and early clinical studies. However, despite these translational efforts, we currently have no immune-based therapies for AML on the market, with the exception of gemtuzumab ozogamicin. In this focused review, we discuss molecular target validation and the most relevant clinical updates for immune-based experimental therapeutics including anti-CD47 monoclonal antibodies, CAR-T therapies, and bispecific T cell engagers. We highlight barriers to the clinical translation of these therapies in AML, and we propose solutions to optimize the manufacturing and delivery of the most novel immune-based therapies in the pipeline.

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