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  Genome-wide DNA methylation events in TMPRSS2-ERG fusion-negative prostate cancers implicate an EZH2-dependent mechanism with miR-26a hypermethylation

Börno, S., Fischer, A., Kerick, M., Falth, M., Laible, M., Brase, J. C., et al. (2012). Genome-wide DNA methylation events in TMPRSS2-ERG fusion-negative prostate cancers implicate an EZH2-dependent mechanism with miR-26a hypermethylation. Cancer Discovery, 2(11), 1024-1035. doi:10.1158/2159-8290.CD-12-0041.

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Börno, S.1, Autor           
Fischer, A.1, Autor           
Kerick, M.1, Autor           
Falth, M., Autor
Laible, M., Autor
Brase, J. C., Autor
Kuner, R., Autor
Dahl, A., Autor
Grimm, C.2, Autor           
Sayanjali, B., Autor
Isau, M.1, Autor           
Röhr, C.1, Autor           
Wunderlich, A.1, Autor           
Timmermann, B.3, Autor           
Claus, R., Autor
Plass, C., Autor
Graefen, M., Autor
Simon, R., Autor
Demichelis, F., Autor
Rubin, M. A., Autor
Sauter, G., AutorSchlomm, T., AutorSültmann, H., AutorLehrach, H.4, Autor           Schweiger, M. R.1, Autor            mehr..
Affiliations:
1Cancer Genomics (Michal-Ruth Schweiger), Dept. of Vertebrate Genomics (Head: Hans Lehrach), Max Planck Institute for Molecular Genetics, Max Planck Society, Berlin, Germany, ou_1479649              
2In vitro Ligand Screening (Zoltán Konthur), Dept. of Vertebrate Genomics (Head: Hans Lehrach), Max Planck Institute for Molecular Genetics, Max Planck Society, Berlin, Germany, ou_1479653              
3Sequencing, Max Planck Institute for Molecular Genetics, Max Planck Society, Berlin, Germany, ou_1433559              
4Dept. of Vertebrate Genomics (Head: Hans Lehrach), Max Planck Institute for Molecular Genetics, Max Planck Society, Berlin, Germany, ou_1433550              

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 Zusammenfassung: Prostate cancer is the second most common cancer among men worldwide. Alterations in the DNA methylation pattern can be one of the leading causes for prostate cancer formation. This study is the first high-throughput sequencing study investigating genome-wide DNA methylation patterns in a large cohort of 51 tumor and 53 benign prostate samples using methylated DNA immunoprecipitation sequencing. Comparative analyses identified more than 147,000 cancer-associated epigenetic alterations. In addition, global methylation patterns show significant differences based on the TMPRSS2-ERG rearrangement status. We propose the hypermethylation of miR-26a as an alternative pathway of ERG rearrangement-independent EZH2 activation. The observed increase in differential methylation events in fusion-negative tumors can explain the tumorigenic process in the absence of genomic rearrangements. SIGNIFICANCE: In contrast to TMPRSS2-ERG -rearranged tumors, the pathomechanism for gene fusion-negative tumors is completely unclear. Using a sequencing-based approach, our work uncovers significant global epigenetic alterations in TMPRSS2-ERG gene fusion-negative tumors and provides a mechanistic explanation for the tumor formation process.

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 Datum: 2012-08-282012-11
 Publikationsstatus: Erschienen
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 Art der Begutachtung: Expertenbegutachtung
 Identifikatoren: DOI: 10.1158/2159-8290.CD-12-0041
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Titel: Cancer Discovery
Genre der Quelle: Zeitschrift
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Ort, Verlag, Ausgabe: -
Seiten: - Band / Heft: 2 (11) Artikelnummer: - Start- / Endseite: 1024 - 1035 Identifikator: -