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慢性髓性白血病的免疫分类可区分慢性期、即将发生的原始细胞转化期和急性淋巴细胞白血病。

Immunological classification of chronic myeloid leukemia distinguishes chronic phase, imminent blastic transformation, and acute lymphoblastic leukemia.

作者信息

Schmetzer H M, Gerhartz H H

机构信息

Med.Dept.III, Klinikum Grosshadern, Munich.

出版信息

Exp Hematol. 1997 Jun;25(6):502-8.

PMID:9197328
Abstract

The clinical course of chronic myeloid leukemia (CML) is highly variable and therefore it is difficult to predict the duration of the chronic phase. We studied the immunological expression of maturation patterns in 62 cases of CML (30 cases in clinical/cytological blast crisis (BC), 32 cases in clinical/cytological chronic phase (CP) by means of a double marker enzyme immuno assay (DM-EIA). Immunological findings were supplemented by Southern blots using Ig-JH-, TCRbeta- and bcr-probes. Patients in BC (n = 30) expressed high proportions of CD10, CD20, CD33, CD34 and low degrees of a mature myeloid marker (CD15). Myeloid BC bone marrow (BM) cells showed a high degree of coexpression of unusual, lineage restricted markers: 25% of CD15-positive cells also expressed markers like CD10, CD20 or CD34. In contrast, BM cells in lymphoid BC did not show this coexpression. In CP two groups were distinguished immunologically: concordant cases which were immunologically normal (n = 14) and discordant cases (n = 18) which showed increased proportions of unusual, lineage restricted markers and double labelled cells (e.g. CD15/CD34). The latter group developed clinical BC earlier during further follow up (p = 0.009). Cases of lymphoid BC (n = 11)--in contrast to acute lymphoblastic leukemia (ALL) patients (n = 21)--did not show coexpression of CD15/CD10, CD20, CD34. These data show that blast clones can be detected in CML-CP by characteristic immunological maturation defects several months before the clinical onset of BC. Moreover, the lymphoid "blasts" of CML-BC represent a relatively differentiated lymphoid population of cells which can be distinguished from ALL by their lack of coexpression of unusual, lineage restricted markers.

摘要

慢性髓性白血病(CML)的临床病程高度可变,因此很难预测慢性期的持续时间。我们通过双标记酶免疫分析(DM-EIA)研究了62例CML患者(30例处于临床/细胞学急变期(BC),32例处于临床/细胞学慢性期(CP))成熟模式的免疫表达。免疫结果通过使用Ig-JH、TCRβ和bcr探针的Southern印迹进行补充。处于BC期的患者(n = 30)高比例表达CD10、CD20、CD33、CD34,而成熟髓系标志物(CD15)表达程度较低。髓系BC期骨髓(BM)细胞显示出异常的、谱系限制性标志物的高度共表达:25%的CD15阳性细胞也表达如CD10、CD20或CD34等标志物。相比之下,淋巴系BC期的BM细胞未显示这种共表达。在CP期,根据免疫情况分为两组:免疫正常的一致病例(n = 14)和显示异常谱系限制性标志物及双标记细胞(如CD15/CD34)比例增加的不一致病例(n = 18)。后一组在进一步随访期间更早发展为临床BC期(p = 0.009)。与急性淋巴细胞白血病(ALL)患者(n = 21)相比,淋巴系BC期病例(n = 11)未显示CD15/CD10、CD20、CD34的共表达。这些数据表明,在BC临床发作前数月,通过特征性免疫成熟缺陷可在CML-CP期检测到原始克隆。此外,CML-BC的淋巴系“原始细胞”代表了一个相对分化的淋巴细胞群体,可通过其缺乏异常谱系限制性标志物的共表达与ALL区分开来。

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