A novel chromosomal translocation t(3;7)(q26;q21) in myeloid leukemia resulting in overexpression of EVI1
作者： C. T. Storlazzi , L. Anelli , F. Albano , A. Zagaria , M. Ventura
DOI: 10.1007/S00277-003-0778-Y
关键词: RUNX1T1 、 homeobox A9 、 ABL 、 Leukemia 、 Fusion gene 、 Biology 、 Chromosomal translocation 、 Fusion transcript 、 Myeloid leukemia 、 Molecular biology
摘要: The EVI1 proto-oncogene encodes a nuclear zinc finger protein that acts as transcription repressor factor. In myeloid leukemia it is often activated by chromosomal rearrangements involving band 3q26, where the gene has been mapped. Here we report two cases [a chronic blast crisis (CML-BC) and an acute (AML) M4] showing t(3;7)(q26;q21) translocation in balanced unbalanced form, respectively. Fluorescent situ hybridization (FISH) analysis revealed both patients showed breakpoint on chromosome 3 inside clone RP11–33A1 containing oncogene and, 7, RP11–322M5, partially CDK6 which D cyclin-dependent kinase gene, observed to be overexpressed disrupted many hematological malignancies. Reverse transcriptase polymerase chain reaction (RT-PCR) overexpression of cases, but excluded presence any CDK6/EVI1 fusion transcript. expression was also detected. Together, these data indicate activation likely due not generation novel with position effect dysregulating its transcriptional pattern.
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