| Literature DB >> 17620387 |
Tony L Ng1, Maureen J O'Sullivan, Catherine J Pallen, Malcolm Hayes, Paul W Clarkson, Mark Winstanley, Poul H B Sorensen, Torsten O Nielsen, Douglas E Horsman.
Abstract
Ewing family tumors are molecularly characterized by expression of chimeric transcripts generated by specific chromosomal translocations, most commonly involving fusion of the EWS gene to a member of the ETS family of transcription factors (including FLI1, ERG, ETV1, E1AF, and FEV). Approximately 85% of reported cases of Ewing sarcoma bear an EWS-FLI1 fusion. In rare cases, FUS can substitute for EWS, with translocation t(16;21)(p11;q24) producing a FUS-ERG fusion with no EWS rearrangement. We report a case of Ewing sarcoma, presenting as a pathological fracture of the distal clavicle in a 33-year-old male, in which cytogenetic analysis revealed a single t(2;16)(q35;p11) balanced translocation. Fluorescence in situ hybridization using a commercially available diagnostic probe was negative for an EWS gene rearrangement; instead, break-apart fluorescence in situ hybridization probes for FUS and FEV were positive for a translocation involving these genes. Cloning and sequencing of the breakpoint region demonstrated an in-frame fusion of FUS to FEV. In conclusion, this represents the first reported case of Ewing family tumors demonstrating a variant translocation involving FUS and FEV and highlights the need to consider alternative permutations of fusion partners for molecular diagnosis of sarcomas.Entities:
Mesh:
Substances:
Year: 2007 PMID: 17620387 PMCID: PMC1975098 DOI: 10.2353/jmoldx.2007.070009
Source DB: PubMed Journal: J Mol Diagn ISSN: 1525-1578 Impact factor: 5.568