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继发性白血病中的(3;21)(q26;q22)易位。两例报告及文献复习。

Translocation (3;21)(q26;q22) in secondary leukemia. Report of two cases and literature review.

作者信息

Schneider N R, Bowman W P, Frenkel E P

机构信息

Department of Pathology, University of Texas Southwestern Medical Center, Dallas 75235-9072.

出版信息

Ann Genet. 1991;34(3-4):256-63.

PMID:1809236
Abstract

The authors report two cases of secondary myelodysplasia and acute myeloid leukemia with t(3;21)(q26.3;q22) as the only cytogenetic abnormality in neoplastic bone marrow. This translocation was identified as a rare, recurring, non-random aberration in chronic myeloid leukemia less than five years ago and in secondary acute myeloid leukemia and myelodysplasia in 1990. The known and suspected cases in the literature are reviewed.

摘要

作者报告了两例继发性骨髓发育异常和急性髓系白血病病例,其肿瘤性骨髓中唯一的细胞遗传学异常为t(3;21)(q26.3;q22)。这种易位在不到五年前被确定为慢性髓系白血病中一种罕见的、反复出现的、非随机的畸变,在1990年被确定为继发性急性髓系白血病和骨髓发育异常中的畸变。本文对文献中已知和疑似的病例进行了综述。

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Ann Genet. 1991;34(3-4):256-63.
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引用本文的文献

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Generation of the AML1-EVI-1 fusion gene in the t(3;21)(q26;q22) causes blastic crisis in chronic myelocytic leukemia.t(3;21)(q26;q22)中AML1-EVI-1融合基因的产生导致慢性粒细胞白血病发生原始细胞危象。
EMBO J. 1994 Feb 1;13(3):504-10. doi: 10.1002/j.1460-2075.1994.tb06288.x.
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Dual functions of the AML1/Evi-1 chimeric protein in the mechanism of leukemogenesis in t(3;21) leukemias.AML1/Evi-1嵌合蛋白在t(3;21)白血病白血病发生机制中的双重作用。
Mol Cell Biol. 1995 May;15(5):2383-92. doi: 10.1128/MCB.15.5.2383.