MECOM (EVI1)重排:2例MDS患者复杂3q反转/缺失的回顾和病例报告。

Helen Lawce, Elina Szabo, Yumi Torimaru, Craig Davis, Karin Osterberg, Susan Olson, Steve Moore
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摘要

带有inv(3)/t(3;3)(q13q25)的急性骨髓性白血病(AML)与干细胞调节因子MECOM(又名EVI1)的异常表达相关。OHSU Knight诊断实验室(KDL)细胞遗传学实验室收到的两个骨髓样本,用于染色体和FISH,用于骨髓增生异常综合征(MDS)向AML进展的问题,显示复杂的异常,包括染色体3q缺失,一个带有del(3)(q13q25),另一个带有del(3)(q22q25)。考虑到MECOM癌基因的激活以及与经典3q染色体反转同时发生的GATA2抑癌基因失活对预后的重要性,我们使用两种不同的探针设计进行了荧光原位杂交(FISH),以更好地确定这两种情况下的3q缺失。使用Abbott Molecular Laboratories双融合MECOM/RPN1探针,两名患者的间期和中期细胞均显示出与融合和缺失一致的变异单融合(橙色/绿色/融合)信号模式。使用三色(红/绿/aqua) Cytocell EVI1探针,两种情况下的间期细胞均显示红/绿分裂信号,而aqua信号与绿色信号保持一致。分裂信号之间的距离通常小于通常描述的倒位染色体3。因此,这些发现与染色体3q的复杂反转和并发缺失一致。因此,这两例患者骨髓中g带染色体的3q缺失与MECOM的激活和GATA2的失活最为一致。
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MECOM (EVI1) Rearrangements: A Review and Case Report of Two MDS Patients with Complex 3q Inversion/Deletions.

Acute myelogeneous leukemia (AML) with inv(3)/t(3;3)(q13q25) is associated with aberrant expression of the stem-cell regulator MECOM (aka EVI1). Two bone marrow samples received in the OHSU Knight Diagnostic Laboratories (KDL) Cytogenetics Laboratory for chromosomes and FISH for a question of progression of myelodysplastic syndrome (MDS) to AML showed complex abnormalities including a deletion of chromosome 3q, one with del(3)(q13q25) and the other with del(3)(q22q25). In light of the prognostic importance of the activation of the MECOM oncogene and the concurrent inactivation of the GATA2 tumor suppressor that occurs with the classic inversion of chromosome 3q, fluorescence in situ hybridization (FISH) was performed using two different probe designs to better define the 3q deletions in the two cases. Using the Abbott Molecular Laboratories dual fusion MECOM/RPN1 probe, interphase and metaphase cells in both patients showed a variant single fusion (orange/green/fusion) signal pattern consistent with fusion and deletion. Using the three-color (red/green/aqua) Cytocell EVI1 probe, interphase cells in both cases showed a split red/green signal with the aqua signal remaining with the green signal. The distance between the split signals was generally less than is usually seen in the commonly described inverted chromosome 3. These findings are therefore consistent with a complex inversion and concurrent deletion/deletions of chromosome 3q. Thus, the deletion 3q seen in G-banded chromosomes from bone marrow from these two patients is most consistent with the activation of MECOM and the inactivation of GATA2.

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