Disruption of the ETV6 gene as a consequence of a rare translocation (12;12)(p13;q13) in treatment-induced acute myeloid leukemia after breast cancer

被引：7
|
作者：
Manola, Kalliopi N. [1 ]
Georgakakos, Vasileios N. [1 ]
Margaritis, Dimitris [2 ]
Stavropoulou, Chryssa [1 ]
Panos, Christos [1 ]
Kotsianidis, Loarmis [2 ]
Panteliasa, Gabriel E. [1 ]
Sambani, Constantina [1 ]
机构：
[1] Demokritos Natl Ctr Sci Res, Lab Cytogenet, GR-15310 Athens, Greece
[2] Democritus Univ Thrace, Sch Med, Dept Hematol, GR-68100 Alexandroupolis, Greece
来源：
CANCER GENETICS AND CYTOGENETICS | 2008年 / 180卷 / 01期
关键词：
D O I：
10.1016/j.cancergencyto.2007.09.004
中图分类号：
R73 [肿瘤学];
学科分类号：
100214 ;
摘要：
We describe a case of treatment-induced acute myeloid leukemia M2 after breast cancer with a rare reciprocal t(12;12)(p13;q13) as a secondary cytogenetic abnormality in addition to the t(11;19)(q23;p13.1). Fluorescence in situ hybridization analysis revealed that both ETV6 genes (previously TEL) were located on the same der(12)t(12;12) as a result of t(12;12). Interestingly, the translocated ETV6 gene was disrupted, indicating the breakpoint on the large der(12)t(12;12) to be within the ETV6 gene and thus the possible formation of a new fusion gene. CHOP gene at 12q13, was found to be translocated intact to the other homologue chromosome 12, indicating that the breakpoint on the small der(12) is proximal to CHOP. To the best of our knowledge, our patient represents the first report of the rare t(12;12)(p13;q13) described in treatment-induced leukemia and the possible formation of a new fusion gene. (C) 2008 Elsevier Inc. All rights reserved.
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收藏
页码：37 / 42
页数：6
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