Paulus Aneel, Malavasi Fabio, Chanan-Khan Asher
Department of Hematology-Oncology, Mayo Clinic Florida, Jacksonville, FL, USA.
Department of Cancer Biology, Mayo Clinic, Jacksonville, FL, USA.
Leuk Lymphoma. 2022 Oct;63(10):2265-2275. doi: 10.1080/10428194.2022.2090551. Epub 2022 Aug 17.
CD38 is a glycoprotein expressed on chronic lymphocytic leukemia (CLL) cells, which functions to amplify B-cell receptor signaling and regulate nicotinamide adenine dinucleotide metabolism. Increased CD38 expression on CLL cells is associated with an unfavorable disease course, resulting in shorter overall survival. While the role of CD38 as a negative prognostic marker in CLL has been established for over two decades, the therapeutic benefit to be derived by patients from its inhibition has, till date remained an unresolved subject. With the development of high-affinity anti-CD38 targeting drugs, tremendous insight has been gained on which functions of CD38 are detrimental to CLL cell survival as well as the mechanisms of leukemic cell death engaged by these anti-CD38 agents. The current review attempts to resolve how the enzyamtic and receptorial functions of CD38 contribute to CLL pathogenesis, our ability to exploit these functions for immunotherapeutic effect and development of novel strategies targeting CD38.
CD38是一种在慢性淋巴细胞白血病(CLL)细胞上表达的糖蛋白,其作用是放大B细胞受体信号传导并调节烟酰胺腺嘌呤二核苷酸代谢。CLL细胞上CD38表达增加与不良病程相关,导致总生存期缩短。虽然CD38作为CLL阴性预后标志物的作用已确立二十多年,但迄今为止,患者从其抑制中获得的治疗益处仍是一个未解决的问题。随着高亲和力抗CD38靶向药物的发展,人们对CD38的哪些功能对CLL细胞存活有害以及这些抗CD38药物导致白血病细胞死亡的机制有了深刻的认识。本综述试图阐明CD38的酶促和受体功能如何促成CLL发病机制,我们利用这些功能实现免疫治疗效果的能力以及靶向CD38的新策略的开发。