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1 Department of Pathology, Brigham and Women's Hospital; 2 Harvard Medical School; 3 Dana-Farber Cancer Institute, Boston, Massachusetts; 4 Department of Pathology, University of Ulm; 5 Department of Urology, University Hospital Ulm, Ulm, Germany; 6 Bioinformatics Group, SRA Division, ITC-irst, Trento, Italy; 7 Broad Institute of Harvard and Massachusetts Institute of Technology, Cambridge, Massachusetts; Departments of 8 Pathology, 9 Urology, and 10 Medical Oncology, University of Michigan, Ann Arbor, Michigan; and 11 University of Washington, Seattle, Washington
Requests for reprints: Mark A. Rubin, Department of Pathology, Brigham and Women's Hospital/Harvard Medical School, EBRC 442A, 221 Longwood Avenue, Boston, MA 02115-6110. Phone: 617-525-6700; Fax: 617-264-6898; E-mail: marubin{at}partners.org.
Prostate cancer is a common and clinically heterogeneous disease with marked variability in progression. The recent identification of gene fusions of the 5'-untranslated region of TMPRSS2 (21q22.3) with the ETS transcription factor family members, either ERG (21q22.2), ETV1 (7p21.2), or ETV4 (17q21), suggests a mechanism for overexpression of the ETS genes in the majority of prostate cancers. In the current study using fluorescence in situ hybridization (FISH), we identified the TMPRSS2:ERG rearrangements in 49.2% of 118 primary prostate cancers and 41.2% of 18 hormone-naive lymph node metastases. The FISH assay detected intronic deletions between ERG and TMPRSS2 resulting in TMPRSS2:ERG fusion in 60.3% (35 of 58) of the primary TMPRSS2:ERG prostate cancers and 42.9% (3 of 7) of the TMPRSS2:ERG hormone-naive lymph node metastases. A significant association was observed between TMPRSS2:ERG rearranged tumors through deletions and higher tumor stage and the presence of metastatic disease involving pelvic lymph nodes. Using 100K oligonucleotide single nucleotide polymorphism arrays, a homogeneous deletion site between ERG and TMPRSS2 on chromosome 21q22.2-3 was identified with two distinct subclasses distinguished by the start point of the deletion at either 38.765 or 38.911 Mb. This study confirms that TMPRSS2:ERG is fused in approximately half of the prostate cancers through deletion of genomic DNA between ERG and TMPRSS2. The deletion as cause of TMPRSS2:ERG fusion is associated with clinical features for prostate cancer progression compared with tumors that lack the TMPRSS2:ERG rearrangement. (Cancer Res 2006; 66(17): 8337-41)
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