Recurrent rearrangements of FOS and FOSB define osteoblastoma

Matthew W. Fittall, William Mifsud, Nischalan Pillay, Hongtao Ye, Anna-Christina Strobl, Annelien Verfaillie, Jonas Demeulemeester, Lei Zhang, Fitim Berisha, Maxime Tarabichi, Matthew D. Young, Elena Miranda, Patrick S. Tarpey, Roberto Tirabosco, Fernanda Amary, Agamemnon E. Grigoriadis, Michael R. Stratton, Peter Loo, Cristina R. Antonescu, Peter J. Campbell, Adrienne M. Flanagan () and Sam Behjati ()
Additional contact information
Matthew W. Fittall: The Francis Crick Institute
William Mifsud: University College London Cancer Institute
Nischalan Pillay: University College London Cancer Institute
Hongtao Ye: Royal National Orthopaedic Hospital NHS Trust
Anna-Christina Strobl: Royal National Orthopaedic Hospital NHS Trust
Annelien Verfaillie: The Francis Crick Institute
Jonas Demeulemeester: The Francis Crick Institute
Lei Zhang: Memorial Sloan Kettering Cancer Center
Fitim Berisha: Royal National Orthopaedic Hospital NHS Trust
Maxime Tarabichi: The Francis Crick Institute
Matthew D. Young: Wellcome Trust Sanger Institute
Elena Miranda: University College London Cancer Institute
Patrick S. Tarpey: Wellcome Trust Sanger Institute
Roberto Tirabosco: Royal National Orthopaedic Hospital NHS Trust
Fernanda Amary: Royal National Orthopaedic Hospital NHS Trust
Agamemnon E. Grigoriadis: Guy’s Hospital
Michael R. Stratton: Wellcome Trust Sanger Institute
Peter Loo: The Francis Crick Institute
Cristina R. Antonescu: Memorial Sloan Kettering Cancer Center
Peter J. Campbell: Wellcome Trust Sanger Institute
Adrienne M. Flanagan: University College London Cancer Institute
Sam Behjati: Wellcome Trust Sanger Institute

Nature Communications, 2018, vol. 9, issue 1, 1-6

Abstract: Abstract The transcription factor FOS has long been implicated in the pathogenesis of bone tumours, following the discovery that the viral homologue, v-fos, caused osteosarcoma in laboratory mice. However, mutations of FOS have not been found in human bone-forming tumours. Here, we report recurrent rearrangement of FOS and its paralogue, FOSB, in the most common benign tumours of bone, osteoblastoma and osteoid osteoma. Combining whole-genome DNA and RNA sequences, we find rearrangement of FOS in five tumours and of FOSB in one tumour. Extending our findings into a cohort of 55 cases, using FISH and immunohistochemistry, provide evidence of ubiquitous mutation of FOS or FOSB in osteoblastoma and osteoid osteoma. Overall, our findings reveal a human bone tumour defined by mutations of FOS and FOSB.

Date: 2018
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DOI: 10.1038/s41467-018-04530-z

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