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TMPRSS2:ERG fusion-associated deletions provide insight into the heterogeneity of prostate cancer.

TMPRSS2:ERG fusion-associated deletions provide insight into the heterogeneity of prostate cancer. Research Abstract Details 

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  • TMPRSS2:ERG fusion-associated deletions provide insight into the heterogeneity of prostate cancer. Abstract Text:

    sven pernerSven Perner,francesca demichelisFrancesca Demichelis,rameen beroukhimRameen Beroukhim,folke h schmidtFolke H Schmidt,juan-miguel mosqueraJuan-Miguel Mosquera,sunita setlurSunita Setlur,joelle tchindaJoelle Tchinda,scott a tomlinsScott A Tomlins,matthias d hoferMatthias D Hofer,kenneth g pientaKenneth G Pienta,rainer kueferRainer Kuefer,robert vessellaRobert Vessella,xiao-wei sunXiao-Wei Sun,matthew meyersonMatthew Meyerson,charles leeCharles Lee,william r sellersWilliam R Sellers,arul m chinnaiyanArul M Chinnaiyan,mark a rubinMark A Rubin,

    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.

    TMPRSS2:ERG fusion-associated deletions provide insight into the heterogeneity of prostate cancer. Publishing Authors By Initials

    s pernerS Perner,f demichelisF Demichelis,r beroukhimR Beroukhim,fh schmidtFH Schmidt,jm mosqueraJM Mosquera,s setlurS Setlur,j tchindaJ Tchinda,sa tomlinsSA Tomlins,md hoferMD Hofer,kg pientaKG Pienta,r kueferR Kuefer,r vessellaR Vessella,xw sunXW Sun,m meyersonM Meyerson,c leeC Lee,wr sellersWR Sellers,am chinnaiyanAM Chinnaiyan,ma rubinMA Rubin,

    For similar abstracts research abstracts see: abstracts research

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    TMPRSS2:ERG fusion-associated deletions provide insight into the heterogeneity of prostate cancer. Journal Published:

    PUBLICATION TYPE: Research Support, U.S. Gov't,

    Journal: Cancer research

    VOLUME: 66

    Page Numbers: 8337-41

    Journal Abbreviation:

    ISSN: 1538-7445

    DAY: 1

    MONTH: Sep

    YEAR: 2006

    TMPRSS2:ERG fusion-associated deletions provide insight into the heterogeneity of prostate cancer. Information

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    LANGUAGE: eng

    NlmUniqueID: 2984705

    TMPRSS2:ERG fusion-associated deletions provide insight into the heterogeneity of prostate cancer. Keywords Mesh Terms:

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    Grant and Affiliation Information for TMPRSS2:ERG fusion-associated deletions provide insight into the heterogeneity of prostate cancer.

    AFFILIATION: Department of Pathology, Brigham and Women's Hospital, Harvard Medical School, EBRC 442A, 221 Longwood Avenue, Boston, MA 02115-6110, USA.

    Country: United States

    United States Research PublicationUnited States Research Publication

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    MEDLINETA: Cancer Res

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