Pathology and Forensic Medicine, Baghdad University College of Medicine, Baghdad, Iraq.
Pathology and Forensic Medicine, Al-Nahrain University Medical College, Baghdad, Iraq.
Cardiovasc Hematol Disord Drug Targets. 2020;20(2):145-151. doi: 10.2174/1871529X19666190719105954.
Laboratory data suggest that acute myeloid leukemia AML originates from a rare population of cells, termed Leukemic Stem Cells (LSCs) or leukemia-initiating cells, which are capable of self-renewal, proliferation and differentiation into malignant blasts. There is a universal agreement that LSCs lie within the CD34+ compartment of hemopoietic cells and most of leukemic stem cells express the interleukin-3 alpha chain receptor, CD123 and lack CD38. This study aimed to estimate the expression of LSC phenotype in AML patients and to correlate it with response to induction therapy.
A cohort of 41 patients older than 15 years with newly diagnosed de novo AML were enrolled in this study. They were obtained from the National center of hematology in Baghdad and Baghdad teaching hospital between February and July 2013. The expression of CD34, CD38 and CD123 was assessed by multi-color flow cytometry. LSC positive (LSC+) samples must express CD34 and CD123 and lack the expression of CD38 in >1% of cells. French American British (FAB) classification system was used in this study. After four weeks of induction therapy; three groups were found: those who reached the Complete morphological Remission (CR), those who failed to reach CR and those who died before the assessment of morphological remission. The last two groups were merged for statistical purposes.
After the course of induction therapy, 41.46% of patients had complete morphological remission while 58.54% of the studied patients failed to reach complete remission. The Complete Remission (CR) rate was higher (53.33%) in patients who were negative for LSC phenotype than patients who were positive for LSC phenotype (34.61%).
LSCs were expressed in 63.41% of AML cases and were in approximate distribution in FAB M3 and non-M3 patients. The expression of LSC phenotype was associated with poor response to induction therapy in AML patients.
实验室数据表明，急性髓系白血病（AML）起源于一种罕见的细胞群体，称为白血病干细胞（LSCs）或白血病起始细胞，它们能够自我更新、增殖并分化为恶性细胞。人们普遍认为，LSCs 存在于造血细胞的 CD34+ 隔室中，大多数白血病干细胞表达白细胞介素-3 受体α链（CD123），缺乏 CD38。本研究旨在评估 AML 患者中 LSC 表型的表达，并将其与诱导治疗的反应相关联。
本研究纳入了 2013 年 2 月至 7 月间在伊拉克巴格达国家血液学中心和巴格达教学医院新诊断为初发 AML 的 41 例年龄大于 15 岁的患者。采用多色流式细胞术评估 CD34、CD38 和 CD123 的表达。LSC 阳性（LSC+）样本必须在>1%的细胞中表达 CD34 和 CD123，且缺乏 CD38 的表达。本研究采用法国-美国-英国（FAB）分类系统。在诱导治疗 4 周后，发现了以下三组：达到完全形态缓解（CR）的患者、未能达到 CR 的患者和在形态缓解评估前死亡的患者。出于统计目的，将后两组合并。
在诱导治疗后，41.46%的患者达到完全形态缓解，而 58.54%的研究患者未能达到完全缓解。LSC 表型阴性的患者完全缓解（CR）率（53.33%）高于 LSC 表型阳性的患者（34.61%）。
在 63.41%的 AML 病例中表达了 LSCs，并且在 FAB M3 和非-M3 患者中的分布大致相同。LSC 表型的表达与 AML 患者对诱导治疗的反应不良相关。
