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Multiple genomic alterations on 21q22 predict various TMPRSS2/ERG fusion transcripts in human prostate cancers.

Multiple genomic alterations on 21q22 predict various TMPRSS2/ERG fusion transcripts in human prostate cancers. Research Abstract Details 

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  • Multiple genomic alterations on 21q22 predict various TMPRSS2/ERG fusion transcripts in human prostate cancers. Abstract Text:

    wennuan liuWennuan Liu,charles m ewingCharles M Ewing,bao-li changBao-Li Chang,tao liTao Li,jishan sunJishan Sun,aubrey r turnerAubrey R Turner,latchezar dimitrovLatchezar Dimitrov,yi zhuYi Zhu,jielin sunJielin Sun,jin woo kimJin Woo Kim,s lilly zhengS Lilly Zheng,william b isaacsWilliam B Isaacs,jianfeng xuJianfeng Xu,

    A number of TMPRSS2/ERG fusion transcripts have been reported since the discovery that recurrent genomic rearrangements result in the fusion of TMPRSS2 and ETS family member genes. In this article we present evidence demonstrating that multiple genomic alterations contribute to the formation of various TMPRSS2/ERG transcripts. Using allele-specific analysis of the data generated from the GeneChip 500K SNP array we observed both hemizygous and homozygous deletions occurring at different locations between and within TMPRSS2 and ERG in prostate cancers. The 500K SNP array enabled us to fine map the start and end of each deletion to specific introns of these two genes, and to predict a variety of fusion transcripts, including a new form which was confirmed by sequence analysis of the fusion transcripts in various tumors. We also inferred that translocation is an additional mechanism of fusion for these two genes in some tumors, based on largely diploid genomic DNA between TMPRSS and ERG, and different fusion transcripts produced in these tumors. Using a bioinformatics approach, we then uncovered the consensus sequences in the regions harboring the breakpoints of the deletions. These consensus sequences were homologous to the human Alu-Sq and Alu-Sp subfamily consensus sequences, with more than 80% homology. The presence/absence of Alu family consensus sequence in the introns of TMPRSS2 and ERG correlates with the presence/absence of fusion transcripts of theses two genes, indicating that these consensus sequences may contribute to genomic deletions and the fusion of TMPRSS2 and ERG in prostate cancer.

    Multiple genomic alterations on 21q22 predict various TMPRSS2/ERG fusion transcripts in human prostate cancers. Publishing Authors By Initials

    w liuW Liu,cm ewingCM Ewing,bl changBL Chang,t liT Li,j sunJ Sun,ar turnerAR Turner,l dimitrovL Dimitrov,y zhuY Zhu,j sunJ Sun,jw kimJW Kim,sl zhengSL Zheng,wb isaacsWB Isaacs,j xuJ Xu,

    For similar proteins: dna-binding proteins: trans-activators research abstracts see: proteins: dna-binding proteins: trans-activators research

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    Multiple genomic alterations on 21q22 predict various TMPRSS2/ERG fusion transcripts in human prostate cancers. Journal Published:

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

    Journal: Genes, chromosomes & cancer

    VOLUME: 46

    Page Numbers: 972-80

    Journal Abbreviation: Genes Chromosomes Cancer

    ISSN: 1045-2257

    DAY: 3

    MONTH: Nov

    YEAR: 2007

    Multiple genomic alterations on 21q22 predict various TMPRSS2/ERG fusion transcripts in human prostate cancers. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 9007329

    Multiple genomic alterations on 21q22 predict various TMPRSS2/ERG fusion transcripts in human prostate cancers. Keywords Mesh Terms:

    KEYWORDS: Trans-Activators

    MESH TERMS: genetics

    Chemical & Substance for Abstract: Multiple genomic alterations on 21q22 predict various TMPRSS2/ERG fusion transcripts in human prostate cancers. Information

    Substance Name: TMPRSS2 protein, human

    Registry Number: EC 3.4.21.-

    Grant and Affiliation Information for Multiple genomic alterations on 21q22 predict various TMPRSS2/ERG fusion transcripts in human prostate cancers.

    AFFILIATION: Center for Human Genomics, Wake Forest University School of Medicine, Winston-Salem, NC 27157, USA.

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NCI

    GRANT: CA95052

    ACRONYM: CA

    MEDLINETA: Genes Chromosomes Cancer

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