Journal
NATURE COMMUNICATIONS
Volume 9, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/s41467-018-04530-z
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Funding
- Wellcome Trust
- Skeletal Cancer Action Trust UK
- Royal National Orthopaedic Hospital NHS Trust
- Rosetrees Trust
- National Institute for Health Research
- UCLH Biomedical Research Centre
- UCL Experimental Cancer Centre
- Francis Crick Institute, from Cancer Research UK [FC001202]
- UK Medical Research Council [FC001202]
- Wellcome Trust [FC001202]
- NIH [P50 CA140146-01, P30 CA008748]
- European Union's Horizon 2020 Research and Innovation programme [MSCA 703594-DECODE]
- European Union's Horizon 2020 Research and Innovation programme postdoctoral fellowship [MSCA 747852-SIOMICS]
- Wellcome Trust Intermediate Clinical Research Fellowship
- St. Baldrick's Foundation Robert J. Arceci International Innovation Award
- Wellcome Trust Senior Clinical Research Fellowship
- CRUK Clinician Scientist Fellowship
- Research Foundation - Flanders, FWO Postdoctoral Fellowship
- NATIONAL CANCER INSTITUTE [P30CA008748, P50CA140146] Funding Source: NIH RePORTER
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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.
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