Despite significant efforts to improve therapies for acute myeloid leukemia (AML), clinical outcomes remain poor. Understanding the mechanisms that regulate the development and maintenance of leukemic stem cells (LSCs) is important to reveal new therapeutic opportunities. We have identified CD97, a member of the adhesion class of G protein–coupled receptors (GPCRs), as a frequently up-regulated antigen on AML blasts that is a critical regulator of blast function. High levels of CD97 correlate with poor prognosis, and silencing of CD97 reduces disease aggressiveness in vivo. These phenotypes are due to CD97’s ability to promote proliferation, survival, and the maintenance of the undifferentiated state in leukemic blasts. Collectively, our data credential CD97 as a promising therapeutic target on LSCs in AML.

尽管为改善急性髓细胞性白血病（AML）的治疗做出了巨大努力，但临床结果仍然很差。了解调节白血病干细胞（LSC）发育和维持的机制对于揭示新的治疗机会很重要。我们已经鉴定出CD97是G蛋白偶联受体（GPCR）粘附类别的成员，它是AML blast上经常被上调的抗原，是blast功能的关键调节剂。高水平的CD97与不良预后相关，而CD97沉默会降低体内疾病的侵袭性。这些表型归因于CD97在白血病母细胞中促进增殖，存活和维持未分化状态的能力。总的来说，我们的数据凭证CD97可作为AML中LSC的有希望的治疗靶标。