EWS/FLI-1 fusion signal inserted into chromosome 11 in one patient with morphologic features of Ewing sarcoma, but lacking t(11;22)

被引：12

作者：

Batanian, JR ^{[1
]}

Bridge, JA

Wickert, R

Vogler, C

Gadre, B

Huang, YF

机构：

[1] Cardinal Glennon Childrens Hosp, Dept Pediat, St Louis, MO USA

[2] St Louis Univ, Sch Med, Dept Pathol, Pediat Res Inst,Cardinal Glennon Childrens Hosp, St Louis, MO USA

[3] Cardinal Glennon Childrens Hosp, Dept Cytogenet, St Louis, MO USA

[4] Univ Nebraska, Med Ctr, Dept Pathol & Microbiol, Omaha, NE USA

[5] Univ Nebraska, Med Ctr, Dept Pediat, Omaha, NE USA

[6] Univ Nebraska, Med Ctr, Dept Orthopaed Surg, Omaha, NE USA

来源：

CANCER GENETICS AND CYTOGENETICS | 2002年 / 133卷 / 01期

关键词：

D O I：

10.1016/S0165-4608(01)00563-5

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

A reciprocal t(11;22) (q24:q12) is found in 85% of Ewing sarcomas (ES) cases. We report a case of a child with ES, in whom trisomy 8 was observed as the sole chromosomal abnormality. Fluorescence in situ hybridization-using a set of probes that localize to 22q12 (EWS) and 11q24 (FLI-1) and usually show the translocation as fusion (red-green) signal on der(22)-showed a fusion signal on der(11) suggesting an insertion as the mechanism that led to the EWS-FLI-1 gene rearrangement. Reverse transcriptase-polymerase p chain reaction studies revealed the presence of two EWS/FL11 fusion gene products. (C) 2002 Elsevier Science Inc. All rights reserved.

引用

页码：72 / 75

页数：4

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