急性白血病的谱系鉴定:免疫学和超微结构技术的相关性。

Hematologic pathology Pub Date : 1995-01-01
R Stasi, G Del Poeta, A Venditti, A Bruno, G Suppo, G Aronica, G Di Carlo, G Papa
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引用次数: 0

摘要

本研究评估了免疫学和超微结构方法在揭示急性白血病(ALs)细胞谱系承诺中的价值。对251例ALs进行了形态学、细胞化学和免疫学表征。髓过氧化物酶(MPO)阳性> 3%被认为是白血病细胞髓系起源的证据,细胞质CD22 (cCD22)表达被认为是b系急性淋巴细胞白血病(ALL)的指征,CD3+(膜或细胞质)病例被归类为T-ALL。当原始细胞在光镜下具有未分化的特征,与至少一种针对骨髓特异性抗原(CD13, CD33, MPO)的抗体反应,并且缺乏CD19, cCD22和c/mCD3时,可以诊断为轻度分化急性髓性白血病(AML-M0)。巨核细胞分化通过CD41和/或CD61的表达得到证实。根据这些标准,209例为急性髓性白血病(AML), 39例为ALL。在45%的AML病例中检测到淋巴抗原的表达,30%的all病例显示髓系抗原。其中一例被认为是真正的双表型白血病,因为骨髓谱系中MPO和CD33的联合表达,以及t细胞谱系中cCD3、CD2和CD5的联合表达。两例缺乏骨髓或淋巴分化的迹象,并通过电镜方法进行了研究。一种显示血小板过氧化物酶(PPO)活性,被归类为巨核母细胞变体,另一种与抗cd33反应,被认为是AML-M0。我们得出结论,光镜和标准免疫方法可以准确地显示超过99%的ALs的谱系定位。结合超微结构分析可以确定几乎所有AL病例的细胞性质。
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Lineage identification of acute leukemias: relevance of immunologic and ultrastructural techniques.

This study assesses the value of immunologic and ultrastructural methods in disclosing the lineage commitment of cells from acute leukemias (ALs). Two hundred and fifty-one ALs were characterized morphologically, cytochemically, and immunologically. Myeloperoxidase (MPO) positivity in > 3% of blasts was regarded as evidence of the myeloid origin of leukemic cells, cytoplasmic CD22 (cCD22) expression was taken as an indication for B-lineage acute lymphoblastic leukemia (ALL), and CD3+ (membrane or cytoplasmic) cases were classified as T-ALL. Diagnosis of minimally differentiated acute myeloid leukemia (AML-M0) was made when blast cells had undifferentiated features by light microscopy, reacted with at least one of the antibodies to myeloid-specific antigens (CD13, CD33, MPO), and lacked CD19, cCD22, and c/mCD3. Megakaryoblastic differentiation was demonstrated by the expression of CD41 and/or CD61. Following these criteria, 209 cases were classified as acute myeloid leukemia (AML) and 39 as ALL. Expression of lymphoid antigens was detected in 45% of AML cases and 30% of ALLs showed myeloid antigens. One case was regarded as a true biphenotypic leukemia because of the combined expression of MPO and CD33 for the myeloid lineage, and cCD3, CD2, and CD5 for the T-cell lineage. Two cases lacked signs of myeloid or lymphoid differentiation and were studied by electron microscopy methods. One displayed platelet peroxidase (PPO) activity and was classified as a megakaryoblastic variant, one other reacted with anti-CD33 and was considered AML-M0. We conclude that light microscopy and standard immunologic methods can accurately demonstrate the lineage orientation in greater than 99% of ALs. Integration with ultrastructural analysis can define the cell nature of virtually all cases of AL.

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Topobiology in hematopoiesis. Progress in antisense therapeutics. Ex vivo expansion of hematopoietic progenitor cells in human cord blood: an effect enhanced by cord blood serum. Lineage identification of acute leukemias: relevance of immunologic and ultrastructural techniques. Bone marrow morphology during induction phase of therapy for acute myeloid leukemia (AML).
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