Hanson C A, Abaza M, Sheldon S, Ross C W, Schnitzer B, Stoolman L M
Department of Pathology, University of Michigan Hospitals, Ann Arbor.
Br J Haematol. 1993 May;84(1):49-60. doi: 10.1111/j.1365-2141.1993.tb03024.x.
The incidence of acute biphenotypic leukaemia has ranged from less than 1% to almost 50% in various reports in the literature. This wide variability may be attributed to a number of reasons including lack of consistent diagnostic criteria, use of various panels of antibodies, and the failure to recognize the lack of lineage specificity of some of the antibodies used. The morphology, cytochemistry, immunophenotype and cytogenetics of acute biphenotypic leukaemias from our institution were studied. The diagnostic criteria took into consideration the morphology of the analysed cells, light scatter characteristics, and evaluation of antibody fluorescence histograms in determining whether the aberrant marker expression was arising from leukaemic blasts or differentiated bone marrow elements. Fifty-two of 746 cases (7%) fulfilled our criteria for acute biphenotypic leukaemias. These included 30 cases of acute lymphoblastic leukaemia (ALL) expressing myeloid antigens, 21 cases of acute myelogenous leukaemia (AML) expressing lymphoid markers, and one case of ALL expressing both B- and T-cell associated antigens. The acute biphenotypic leukaemia cases consisted of four major immunophenotypic subgroups: CD2+ AML (11), CD19+ AML (8), CD13 and/or CD33+ ALL (24), CD11b+ ALL (5) and others (4). Chromosomal analysis was carried out in 42/52 of the acute biphenotypic leukaemia cases; a clonal abnormality was found in 31 of these 42 cases. This study highlights the problems encountered in the diagnosis of acute biphenotypic leukaemia, some of which may be responsible for the wide variation in the reported incidence of this leukaemia. We suggest that the use of strict, uniform diagnostic criteria may help in establishing a more consistent approach towards diagnosis of this leukaemic entity. We also suggest that biphenotypic leukaemia is comprised of biologically different groups of leukaemia based on immunophenotypic and cytogenetic findings.
在文献中的各种报道中，急性双表型白血病的发病率从不到1%到近50%不等。这种广泛的变异性可能归因于多种原因，包括缺乏一致的诊断标准、使用各种抗体组合以及未能认识到所使用的某些抗体缺乏谱系特异性。我们对本机构急性双表型白血病的形态学、细胞化学、免疫表型和细胞遗传学进行了研究。诊断标准考虑了所分析细胞的形态、光散射特征以及在确定异常标志物表达是源自白血病原始细胞还是分化的骨髓成分时对抗体荧光直方图的评估。746例病例中有52例（7%）符合我们的急性双表型白血病标准。其中包括30例表达髓系抗原的急性淋巴细胞白血病（ALL）、21例表达淋巴系标志物的急性髓系白血病（AML）以及1例同时表达B细胞和T细胞相关抗原的ALL。急性双表型白血病病例包括四个主要免疫表型亚组：CD2⁺ AML（11例）、CD19⁺ AML（8例）、CD13和/或CD33⁺ ALL（24例）、CD11b⁺ ALL（5例）以及其他（4例）。对52例急性双表型白血病病例中的42例进行了染色体分析；这42例中的31例发现了克隆性异常。本研究突出了急性双表型白血病诊断中遇到的问题，其中一些问题可能是导致该白血病报道发病率差异较大的原因。我们建议使用严格、统一的诊断标准可能有助于建立一种更一致的方法来诊断这种白血病实体。我们还建议，基于免疫表型和细胞遗传学结果，双表型白血病由生物学上不同的白血病组组成。
