No evidence for deletions of the NBS1 gene in lymphomas

被引:18
|
作者
Stumm, P
von Ruskowsky, A
Siebert, R
Harder, S
Varon, R
Wieacker, P
Schlegelberger, B
机构
[1] Otto Von Guericke Univ, Dept Human Genet, D-39120 Magdeburg, Germany
[2] Univ Kiel, Dept Human Genet, D-24105 Kiel, Germany
[3] Dept Human Genet, D-13353 Berlin, Germany
关键词
D O I
10.1016/S0165-4608(00)00390-3
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Patients with Nijmegen breakage syndrome (NBS) have a high risk to develop malignant diseases. most frequently B-cell lymphomas. The NBS gene product, nibrin, is involved in DNA recombination repair, a function shared with known tumor suppressor genes like BRCA1 and BRCA2. This led us to investigate whether NBS acts as tumor suppressor gene in the development of non-Hodgkin lymphomas. Therefore, we performed fluorescence in situ hybridization analysis using a BAC clone containing the entire NBS1 region on eight B-cell and eight T-cell lymphomas, including one B-cell and two T-cell lymphomas with structural abnormalities of 8q. None of the tumors showed a deletion of the NBS1 gene, demonstrating that deletion of the NBS1 gene is not a major cause or a primary event in tumorigenesis of human B- and T-cell lymphomas. (C) 2001 Elsevier Science Inc. All rights reserved.
引用
收藏
页码:60 / 62
页数:3
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