Combined translocation with ZNF198-FGFR1 gene fusion and deletion of potential tumor suppressors in a myeloproliferative disorder

被引：17

作者：

Etienne, Anne

Gelsi-Boyer, Veronique

Carbuccia, Nadine

Adelaide, Jose

Barba, Gianluca

La Starza, Roberta

Murati, Anne

Eclache, Virginie

Birg, Francoise

Birnbaum, Daniel

Mozziconacci, Marie-Joelle

Mecucci, Cristina

Chaffanet, Max

机构：

[1] INSERM, Inst J Paoli I Calmettes, Ctr Rech Cancerol, Dept Oncol Mol & Hematol Mol,UMR 599, F-13009 Marseille, France

[2] Univ Perugia, Dept Hematol, Policlin Monteluce, I-06123 Perugia, Italy

[3] Hop Avicenne, Hematol Lab, F-93000 Bobigny, France

来源：

CANCER GENETICS AND CYTOGENETICS | 2007年 / 173卷 / 02期

关键词：

D O I：

10.1016/j.cancergencyto.2006.10.004

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Tyrosine kinases activated by mutation or translocation are involved in the chronic phase of myeloproliferative disorders. Complementary or alternative events are not so well characterized. We report here a case of t(8;13) generating a ZNF198-FGFR1 fusion kinase gene on the derivative chromosome 13. ZNF198-FGFR1 mRNA, but not FGFR1-ZNF198, was detected by polymerase chain reaction amplification. By using fluorescence in situ hybridization with BAC clones, we mapped a deletion of about 2 megabases on the derivative chromosome 8, including the reciprocal FGFR1-ZNF198 fusion gene and the surrounding genes from 8p11 and 13q12. Potential tumor suppressor genes affected by the deletion by loss (IFT88, CRYLI, TACCI) or break (LATS2) may participate in the malignant process. (c) 2007 Elsevier Inc. All rights reserved.

引用

页码：154 / 158

页数：5

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