Research ExplorerPublicationsGenome-wide DNA methylation events in TMPRSS2-ERG fusion-neg...

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

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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, Stefan T; Fischer, Axel; Kerick, Martin; Fälth, Maria; Laible, Mark; Brase, Jan C; Kuner, Ruprecht; Dahl, Andreas; Grimm, Christina; Sayanjali, Behnam; Isau, Melanie; Röhr, Christina; Wunderlich, Andrea; Timmermann, Bernd; Claus, Rainer; Plass, Christoph; Graefen, Markus; Simon, Ronald; Demichelis, Francesca; Rubin, Mark A; Sauter, Guido; Schlomm, Thorsten; Sültmann, Holger; Lehrach, Hans; Schweiger, Michal R.

In: CANCER DISCOV, Vol. 2, No. 11, 11, 2012, p. 1024-1035.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Börno, ST, Fischer, A, Kerick, M, Fälth, M, Laible, M, Brase, JC, Kuner, R, Dahl, A, Grimm, C, Sayanjali, B, Isau, M, Röhr, C, Wunderlich, A, Timmermann, B, Claus, R, Plass, C, Graefen, M, Simon, R, Demichelis, F, Rubin, MA, Sauter, G, Schlomm, T, Sültmann, H, Lehrach, H & Schweiger, MR 2012, 'Genome-wide DNA methylation events in TMPRSS2-ERG fusion-negative prostate cancers implicate an EZH2-dependent mechanism with miR-26a hypermethylation.', CANCER DISCOV, vol. 2, no. 11, 11, pp. 1024-1035. <http://www.ncbi.nlm.nih.gov/pubmed/22930729?dopt=Citation>

APA

Börno, S. T., Fischer, A., Kerick, M., Fälth, M., Laible, M., Brase, J. C., Kuner, R., Dahl, A., Grimm, C., Sayanjali, B., Isau, M., Röhr, C., Wunderlich, A., Timmermann, B., Claus, R., Plass, C., Graefen, M., Simon, R., Demichelis, F., ... Schweiger, M. R. (2012). Genome-wide DNA methylation events in TMPRSS2-ERG fusion-negative prostate cancers implicate an EZH2-dependent mechanism with miR-26a hypermethylation. CANCER DISCOV, 2(11), 1024-1035. [11]. http://www.ncbi.nlm.nih.gov/pubmed/22930729?dopt=Citation

Vancouver

Börno ST, Fischer A, Kerick M, Fälth M, Laible M, Brase JC et al. Genome-wide DNA methylation events in TMPRSS2-ERG fusion-negative prostate cancers implicate an EZH2-dependent mechanism with miR-26a hypermethylation. CANCER DISCOV. 2012;2(11):1024-1035. 11.

Bibtex

@article{1486af585428411f828c9948bcaed3a9,
title = "Genome-wide DNA methylation events in TMPRSS2-ERG fusion-negative prostate cancers implicate an EZH2-dependent mechanism with miR-26a hypermethylation.",
abstract = "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.",
keywords = "Humans, Male, Gene Fusion, Transfection, *DNA Methylation, Oncogene Proteins, Fusion/*genetics, Epigenomics, Genome, Human, MicroRNAs/*genetics, Polycomb Repressive Complex 2/*genetics, Prostatic Neoplasms/*genetics/pathology, Humans, Male, Gene Fusion, Transfection, *DNA Methylation, Oncogene Proteins, Fusion/*genetics, Epigenomics, Genome, Human, MicroRNAs/*genetics, Polycomb Repressive Complex 2/*genetics, Prostatic Neoplasms/*genetics/pathology",
author = "B{\"o}rno, {Stefan T} and Axel Fischer and Martin Kerick and Maria F{\"a}lth and Mark Laible and Brase, {Jan C} and Ruprecht Kuner and Andreas Dahl and Christina Grimm and Behnam Sayanjali and Melanie Isau and Christina R{\"o}hr and Andrea Wunderlich and Bernd Timmermann and Rainer Claus and Christoph Plass and Markus Graefen and Ronald Simon and Francesca Demichelis and Rubin, {Mark A} and Guido Sauter and Thorsten Schlomm and Holger S{\"u}ltmann and Hans Lehrach and Schweiger, {Michal R}",
year = "2012",
language = "English",
volume = "2",
pages = "1024--1035",
journal = "CANCER DISCOV",
issn = "2159-8274",
publisher = "American Association for Cancer Research Inc.",
number = "11",

}

RIS

TY - JOUR

T1 - Genome-wide DNA methylation events in TMPRSS2-ERG fusion-negative prostate cancers implicate an EZH2-dependent mechanism with miR-26a hypermethylation.

AU - Börno, Stefan T

AU - Fischer, Axel

AU - Kerick, Martin

AU - Fälth, Maria

AU - Laible, Mark

AU - Brase, Jan C

AU - Kuner, Ruprecht

AU - Dahl, Andreas

AU - Grimm, Christina

AU - Sayanjali, Behnam

AU - Isau, Melanie

AU - Röhr, Christina

AU - Wunderlich, Andrea

AU - Timmermann, Bernd

AU - Claus, Rainer

AU - Plass, Christoph

AU - Graefen, Markus

AU - Simon, Ronald

AU - Demichelis, Francesca

AU - Rubin, Mark A

AU - Sauter, Guido

AU - Schlomm, Thorsten

AU - Sültmann, Holger

AU - Lehrach, Hans

AU - Schweiger, Michal R

PY - 2012

Y1 - 2012

N2 - 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.

AB - 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.

KW - Humans

KW - Male

KW - Gene Fusion

KW - Transfection

KW - DNA Methylation

KW - Oncogene Proteins, Fusion/genetics

KW - Epigenomics

KW - Genome, Human

KW - MicroRNAs/genetics

KW - Polycomb Repressive Complex 2/genetics

KW - Prostatic Neoplasms/genetics/pathology

KW - Humans

KW - Male

KW - Gene Fusion

KW - Transfection

KW - DNA Methylation

KW - Oncogene Proteins, Fusion/genetics

KW - Epigenomics

KW - Genome, Human

KW - MicroRNAs/genetics

KW - Polycomb Repressive Complex 2/genetics

KW - Prostatic Neoplasms/genetics/pathology

M3 - SCORING: Journal article

VL - 2

SP - 1024

EP - 1035

JO - CANCER DISCOV

JF - CANCER DISCOV

SN - 2159-8274

IS - 11

M1 - 11

ER -