%0 Journal Article %1 berger11 %A Berger, Michael F. %A Lawrence, Michael S. %A Demichelis, Francesca %A Drier, Yotam %A Cibulskis, Kristian %A Sivachenko, Andrey Y. %A Sboner, Andrea %A Esgueva, Raquel %A Pflueger, Dorothee %A Sougnez, Carrie %A Onofrio, Robert %A Carter, Scott L. %A Park, Kyung %A Habegger, Lukas %A Ambrogio, Lauren %A Fennell, Timothy %A Parkin, Melissa %A Saksena, Gordon %A Voet, Douglas %A Ramos, Alex H. %A Pugh, Trevor J. %A Wilkinson, Jane %A Fisher, Sheila %A Winckler, Wendy %A Mahan, Scott %A Ardlie, Kristin %A Baldwin, Jennifer %A Simons, Jonathan W. %A Kitabayashi, Naoki %A MacDonald, Theresa Y. %A Kantoff, Philip W. %A Chin, Lynda %A Gabriel, Stacey B. %A Gerstein, Mark B. %A Golub, Todd R. %A Meyerson, Matthew %A Tewari, Ashutosh %A Lander, Eric S. %A Getz, Gad %A Rubin, Mark A. %A Garraway, Levi A. %D 2011 %I Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved. %J Nature %K bioinformatics cancer genomics nature prostate %N 7333 %P 214--220 %R 10.1038/nature09744 %T The genomic complexity of primary human prostate cancer %V 470 %X Prostate cancer is the second most common cause of male cancer deaths in the United States. However, the full range of prostate cancer genomic alterations is incompletely characterized. Here we present the complete sequence of seven primary human prostate cancers and their paired normal counterparts. Several tumours contained complex chains of balanced (that is, &#x02018;copy-neutral&#x02019;) rearrangements that occurred within or adjacent to known cancer genes. Rearrangement breakpoints were enriched near open chromatin, androgen receptor and ERG DNA binding sites in the setting of the ETS gene fusion <i>TMPRSS2&#x02013;ERG</i>, but inversely correlated with these regions in tumours lacking ETS fusions. This observation suggests a link between chromatin or transcriptional regulation and the genesis of genomic aberrations. Three tumours contained rearrangements that disrupted <i>CADM2</i>, and four harboured events disrupting either <i>PTEN</i> (unbalanced events), a prostate tumour suppressor, or <i>MAGI2</i> (balanced events), a PTEN interacting protein not previously implicated in prostate tumorigenesis. Thus, genomic rearrangements may arise from transcriptional or chromatin aberrancies and engage prostate tumorigenic mechanisms.

@article{berger11, abstract = {Prostate cancer is the second most common cause of male cancer deaths in the United States. However, the full range of prostate cancer genomic alterations is incompletely characterized. Here we present the complete sequence of seven primary human prostate cancers and their paired normal counterparts. Several tumours contained complex chains of balanced (that is, &#x02018;copy-neutral&#x02019;) rearrangements that occurred within or adjacent to known cancer genes. Rearrangement breakpoints were enriched near open chromatin, androgen receptor and ERG DNA binding sites in the setting of the ETS gene fusion <i>TMPRSS2&#x02013;ERG</i>, but inversely correlated with these regions in tumours lacking ETS fusions. This observation suggests a link between chromatin or transcriptional regulation and the genesis of genomic aberrations. Three tumours contained rearrangements that disrupted <i>CADM2</i>, and four harboured events disrupting either <i>PTEN</i> (unbalanced events), a prostate tumour suppressor, or <i>MAGI2</i> (balanced events), a PTEN interacting protein not previously implicated in prostate tumorigenesis. Thus, genomic rearrangements may arise from transcriptional or chromatin aberrancies and engage prostate tumorigenic mechanisms.}, added-at = {2016-04-08T14:03:53.000+0200}, author = {Berger, Michael F. and Lawrence, Michael S. and Demichelis, Francesca and Drier, Yotam and Cibulskis, Kristian and Sivachenko, Andrey Y. and Sboner, Andrea and Esgueva, Raquel and Pflueger, Dorothee and Sougnez, Carrie and Onofrio, Robert and Carter, Scott L. and Park, Kyung and Habegger, Lukas and Ambrogio, Lauren and Fennell, Timothy and Parkin, Melissa and Saksena, Gordon and Voet, Douglas and Ramos, Alex H. and Pugh, Trevor J. and Wilkinson, Jane and Fisher, Sheila and Winckler, Wendy and Mahan, Scott and Ardlie, Kristin and Baldwin, Jennifer and Simons, Jonathan W. and Kitabayashi, Naoki and MacDonald, Theresa Y. and Kantoff, Philip W. and Chin, Lynda and Gabriel, Stacey B. and Gerstein, Mark B. and Golub, Todd R. and Meyerson, Matthew and Tewari, Ashutosh and Lander, Eric S. and Getz, Gad and Rubin, Mark A. and Garraway, Levi A.}, biburl = {https://www.bibsonomy.org/bibtex/28a20ee7431f363ce598a7e0c25ec2cb7/ytyoun}, doi = {10.1038/nature09744}, interhash = {f67b516914015236f2fa62490758250b}, intrahash = {8a20ee7431f363ce598a7e0c25ec2cb7}, issn = {00280836}, journal = {Nature}, keywords = {bioinformatics cancer genomics nature prostate}, month = feb, number = 7333, pages = {214--220}, publisher = {Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved.}, timestamp = {2016-05-20T10:19:18.000+0200}, title = {The genomic complexity of primary human prostate cancer}, volume = 470, year = 2011 }