Grand, E.K., Grand, F. H., Chase, A. J., Ross, F.M., Corcoran, M. M., Oscier, D. G. and Cross, N. C.P., 2004. Identification of a novel gene, FGFR1OP2, fused to FGFR1 in 8p11 myeloproliferative syndrome. Genes Chromosomes and Cancer, 40 (1), pp. 78-83.
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Official URL: http://www3.interscience.wiley.com/journal/1076309...
The 8p11 myeloproliferative syndrome (EMS) is an aggressive hematological malignancy caused by the fusion of diverse partner genes to fibroblast growth factor receptor 1 (FGFR1). The partner proteins promote dimerization and ligand-independent activation of FGFR1-encoded tyrosine kinase, deregulating hemopoiesis in a manner analogous to BCR-ABL in chronic myeloid leukemia. Here, we describe the identification of a new FGFR1 fusion gene in a patient who presented with T-cell lymphoblastic lymphoma in conjunction with an acquired ins(12;8)(p11;p11p22). Initial FISH analysis and Southern blotting confirmed that FGFR1 was disrupted. Using 5'-RACE PCR, we identified part of a novel gene, FGFR1OP, at chromosome band 12p11 that was fused to exon 9 of FGFR1.FGFR1OP2 is predicted to be translated into an evolutionarily conserved protein containing coiled-coil domains but no other recognizable motifs. The presence of the chimeric gene was confirmed by RT-PCR, genomic DNA PCR, and FISH. These data further support the central role of deregulated FGFR1 in the pathogenesis of EMS.
|Subjects:||Technology > Medicine and Health|
|Group:||School of Health and Social Care > Centre for Postgraduate Medical Research and Education|
|Deposited By:||INVALID USER|
|Deposited On:||19 Oct 2008 20:33|
|Last Modified:||07 Mar 2013 14:51|
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