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Identification of a novel gene, FGFR1OP2, fused to FGFR1 in 8p11 myeloproliferative syndrome. | LitMetric

AI Article Synopsis

  • - The 8p11 myeloproliferative syndrome (EMS) is a severe blood cancer linked to the fusion of different genes with fibroblast growth factor receptor 1 (FGFR1), leading to the uncontrolled activation of its tyrosine kinase, similar to processes seen in chronic myeloid leukemia with BCR-ABL.
  • - A new FGFR1 fusion gene was discovered in a patient with T-cell lymphoblastic lymphoma, due to an acquired genetic alteration (ins(12;8)(p11;p11p22)), which disrupted the FGFR1 gene.
  • - The novel fusion involves FGFR1 and a gene called FGFR1OP2 found on chromosome 12p11, which

Article Abstract

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, FGFR1OP2, 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.

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Source
http://dx.doi.org/10.1002/gcc.20023DOI Listing

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