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[Cancer Research 64, 1920-1923, March 15, 2004]
© 2004 American Association for Cancer Research

Advances in Brief

USP6 (Tre2) Fusion Oncogenes in Aneurysmal Bone Cyst

Andre M. Oliveira1,2, Bae-Li Hsi1, Stanislawa Weremowicz1, Andrew E. Rosenberg3, Paola Dal Cin1, Nora Joseph1, Julia A. Bridge4, Antonio R. Perez-Atayde5 and Jonathan A. Fletcher1,6

1 Department of Pathology, Brigham and Women’s Hospital, Boston, Massachusetts; 2 Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, Minnesota; 3 Department of Pathology, Massachusetts General Hospital, Boston, Massachusetts; 4 Department of Pathology, University of Nebraska Medical Center, Omaha, Nebraska; 5 Department of Pathology, Children’s Hospital, Boston, Massachusetts; and 6 Department of Pediatric Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts

Aneurysmal bone cyst (ABC) is a locally aggressive osseous lesion that typically occurs during the first two decades of life. ABC was regarded historically as a nonneoplastic process, but recent cytogenetic data have shown clonal rearrangements of chromosomal bands 16q22 and 17p13, indicating a neoplastic basis in at least some ABCs. Herein we show that a recurring ABC chromosomal translocation t(16;17)(q22;p13) creates a fusion gene in which the osteoblast cadherin 11 gene (CDH11) promoter region on 16q22 is juxtaposed to the entire ubiquitin-specific protease USP6 (Tre2) coding sequence on 17p13. CDH11-USP6 fusion transcripts were demonstrated only in ABC with t(16;17) but other ABCs had CDH11 or USP6 rearrangements resulting from alternate cytogenetic mechanisms. CDH11 is expressed strongly in bone, and our findings implicate a novel oncogenic mechanism in which deregulated USP6 transcription results from juxtaposition to the highly active CDH11 promoter.




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Copyright © 2004 by the American Association for Cancer Research.