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在 AML 和 CML 中,CD34+/CD38- 和 CD34+/CD38+ 干细胞和祖细胞中的靶表达谱的描绘。

Delineation of target expression profiles in CD34+/CD38- and CD34+/CD38+ stem and progenitor cells in AML and CML.

机构信息

Ludwig Boltzmann Institute for Hematology and Oncology.

Division of Hematology and Hemostaseology, Department of Internal Medicine I, and.

出版信息

Blood Adv. 2020 Oct 27;4(20):5118-5132. doi: 10.1182/bloodadvances.2020001742.

Abstract

In an attempt to identify novel markers and immunological targets in leukemic stem cells (LSCs) in acute myeloid leukemia (AML) and chronic myeloid leukemia (CML), we screened bone marrow (BM) samples from patients with AML (n = 274) or CML (n = 97) and controls (n = 288) for expression of cell membrane antigens on CD34+/CD38- and CD34+/CD38+ cells by multicolor flow cytometry. In addition, we established messenger RNA expression profiles in purified sorted CD34+/CD38- and CD34+/CD38+ cells using gene array and quantitative polymerase chain reaction. Aberrantly expressed markers were identified in all cohorts. In CML, CD34+/CD38- LSCs exhibited an almost invariable aberration profile, defined as CD25+/CD26+/CD56+/CD93+/IL-1RAP+. By contrast, in patients with AML, CD34+/CD38- cells variably expressed "aberrant" membrane antigens, including CD25 (48%), CD96 (40%), CD371 (CLL-1; 68%), and IL-1RAP (65%). With the exception of a subgroup of FLT3 internal tandem duplication-mutated patients, AML LSCs did not exhibit CD26. All other surface markers and target antigens detected on AML and/or CML LSCs, including CD33, CD44, CD47, CD52, CD105, CD114, CD117, CD133, CD135, CD184, and roundabout-4, were also found on normal BM stem cells. However, several of these surface targets, including CD25, CD33, and CD123, were expressed at higher levels on CD34+/CD38- LSCs compared with normal BM stem cells. Moreover, antibody-mediated immunological targeting through CD33 or CD52 resulted in LSC depletion in vitro and a substantially reduced LSC engraftment in NOD.Cg-PrkdcscidIl2rgtm1Wjl/SzJ (NSG) mice. Together, we have established surface marker and target expression profiles of AML LSCs and CML LSCs, which should facilitate LSC enrichment, diagnostic LSC phenotyping, and development of LSC-eradicating immunotherapies.

摘要

为了鉴定急性髓细胞白血病(AML)和慢性髓细胞白血病(CML)中白血病干细胞(LSCs)的新型标志物和免疫学靶点,我们通过多色流式细胞术筛选了 274 例 AML 患者、97 例 CML 患者和 288 例对照者的骨髓(BM)样本中 CD34+/CD38-和 CD34+/CD38+细胞表面抗原的表达。此外,我们使用基因芯片和定量聚合酶链反应在纯化的分选 CD34+/CD38-和 CD34+/CD38+细胞中建立了信使 RNA 表达谱。在所有队列中都发现了异常表达的标记物。在 CML 中,CD34+/CD38- LSCs 表现出几乎不变的异常表型谱,定义为 CD25+/CD26+/CD56+/CD93+/IL-1RAP+。相比之下,在 AML 患者中,CD34+/CD38-细胞可变地表达“异常”膜抗原,包括 CD25(48%)、CD96(40%)、CD371(CLL-1;68%)和 IL-1RAP(65%)。除了一小部分 FLT3 内部串联重复突变患者外,AML LSCs 不表达 CD26。AML 和/或 CML LSCs 上检测到的所有其他表面标记物和靶抗原,包括 CD33、CD44、CD47、CD52、CD105、CD114、CD117、CD133、CD135、CD184 和 roundabout-4,也存在于正常 BM 干细胞中。然而,与正常 BM 干细胞相比,一些表面靶标,包括 CD25、CD33 和 CD123,在 CD34+/CD38- LSCs 上的表达水平更高。此外,通过 CD33 或 CD52 进行抗体介导的免疫靶向治疗可导致体外 LSC 耗竭,并显著降低 NOD.Cg-PrkdcscidIl2rgtm1Wjl/SzJ(NSG)小鼠中的 LSC 植入。总之,我们已经建立了 AML LSCs 和 CML LSCs 的表面标记物和靶标表达谱,这将有助于 LSC 富集、诊断性 LSC 表型分析以及开发消除 LSC 的免疫疗法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f88c/7594398/52466d54423c/advancesADV2020001742absf1.jpg

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