RT-PCR analysis of acute myeloid leukemia with t(8;16)(p11;p13): identification of a novel MOZ/CBP transcript and absence of CBP/MOZ expression.
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Acetyltransferases↗
Biomedical subjects
Ioannis Panagopoulos
Publications and source records attributed to Ioannis Panagopoulos.
Fusion of the FUS and ATF1 genes in a large, deep-seated angiomatoid fibrous histiocytoma.
We report a case of a large, deep-seated, diagnostically difficult angiomatoid fibrous histiocytoma. The neoplastic cells were positive for vimentin, calponin, CD99, and, focally, for desmin and contained intertwining cytoplasmic processes joined by desmosomelike junctions. Fusion of codon 175 of the gene to codon 110 of the gene was detected by reverse transcription-polymerase chain reaction. Because identical fusion of the and genes has been recently reported in another case of angiomatoid fibrous histiocytoma, fusion of these genes may be characteristic for at least a subset of these tumors.
Activating Transcription Factor 1↗
Fusion of RDC1 with HMGA2 in lipomas as the result of chromosome aberrations involving 2q35-37 and 12q13-15.
Rearrangements of chromosome bands 12q13-15 are frequent in various benign mesenchymal and epithelial tumors, and the gene HMGA2 seems to be the most common target within this chromosome region. In the majority of cases, the rearrangements result in a fusion of the first three exons of HMGA2 with different translocation partners. Despite the large number of HMGA2 mutations that have been reported, very little is known about the fusion partners. In this study, we have characterized a recurrent fusion of the first three exons of HMGA2 5' to the G protein-coupled receptor gene (RDC1) in lipomas with rearrangements involving chromosome bands 2q35-37 and 12q13-15, one of several recurrent chromosomal rearrangements in lipomas. The functional impact of the fusion is truncation of HMGA2, because the RDC1 part contributes with a stop codon one amino acid downstream of the breakpoint. The breakpoint within RDC1 was localized in a previously uncharacterized exon of the gene, and our data suggest that RDC1 is subject to alternative splicing.
Alternative Splicing↗