Ioannis Panagopoulos1, Ingvild Lobmaier2, Ludmila Gorunova3, Sverre Heim3,4. 1. Section for Cancer Cytogenetics, Institute for Cancer Genetics and Informatics, The Norwegian Radium Hospital, Oslo University Hospital, Oslo, Norway ioannis.panagopoulos@rr-research.no. 2. Department of Pathology, the Norwegian Radium Hospital, Oslo University Hospital, Oslo, Norway. 3. Section for Cancer Cytogenetics, Institute for Cancer Genetics and Informatics, The Norwegian Radium Hospital, Oslo University Hospital, Oslo, Norway. 4. Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, Norway.
Abstract
BACKGROUND/AIM: Pseudomyogenic hemangioendothelioma is a rare endothelial tumor. Previous genetic investigations have shown that the tumors carry either a SERPINE1-FOSB or an ACTB-FOSB fusion gene. The aim of the study was to identify FOSB fusions linked with pseudomyogenic hemangioendothelioma. MATERIALS AND METHODS: RNA sequencing, reverse transcription polymerase chain reaction (RT-PCR) and Sanger sequencing analyses were performed on a pseudomyogenic hemangioendothelioma. RESULTS: An in-frame fusion was found between exon 4 of WWTR1 from 3q25 and exon 2 of FOSB from 19q13. The fusion gene not only places FOSB under the control of the WWTR1 promoter, but is predicted to encode a chimeric WWTR1-FOSB transcription factor. CONCLUSION: FOSB may be fused with SERPINE1, ACTB, or WWTR1 in pseudomyogenic hemangioendotheliomas. The resulting overexpression of FOSB fusion is a potentially useful marker that could be helpful in the diagnosis of these tumors. Copyright
BACKGROUND/AIM: Pseudomyogenic hemangioendothelioma is a rare endothelial tumor. Previous genetic investigations have shown that the tumors carry either a SERPINE1-FOSB or an ACTB-FOSB fusion gene. The aim of the study was to identify FOSB fusions linked with pseudomyogenic hemangioendothelioma. MATERIALS AND METHODS: RNA sequencing, reverse transcription polymerase chain reaction (RT-PCR) and Sanger sequencing analyses were performed on a pseudomyogenic hemangioendothelioma. RESULTS: An in-frame fusion was found between exon 4 of WWTR1 from 3q25 and exon 2 of FOSB from 19q13. The fusion gene not only places FOSB under the control of the WWTR1 promoter, but is predicted to encode a chimeric WWTR1-FOSB transcription factor. CONCLUSION:FOSB may be fused with SERPINE1, ACTB, or WWTR1 in pseudomyogenic hemangioendotheliomas. The resulting overexpression of FOSB fusion is a potentially useful marker that could be helpful in the diagnosis of these tumors. Copyright
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