In:
Genes, Chromosomes and Cancer, Wiley, Vol. 42, No. 3 ( 2005-03), p. 320-325
Abstract:
8p11 myeloproliferative syndrome (EMS) is a clinical‐pathologic entity characterized by rearrangements involving the FGFR1 gene, which encodes a receptor tyrosine kinase. These rearrangements invariably lead to aberrant fusion proteins in which the kinase activity is constitutively turned on, with resulting oncogenic properties. In this article, we describe a new translocation in EMS, t(7;8)(q34;p11), in which the FGFR1 gene is fused to a previously unidentified partner, the TIF1 gene. We show that both the TIF1–FGFR1 and FGFR1–TIF1 fusion proteins have the potential to be translated as a result of the translocation. Thus, our data extend the involvement of FGFR1 in EMS and lend support to the concept that there is a precise correlation between genotype and phenotype in this disease. © 2004 Wiley‐Liss, Inc.
Type of Medium:
Online Resource
ISSN:
1045-2257
,
1098-2264
Language:
English
Publisher:
Wiley
Publication Date:
2005
detail.hit.zdb_id:
1018988-9
detail.hit.zdb_id:
1492641-6
SSG:
12
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