Integrative genomic analyses reveal an androgen-driven somatic alteration 
landscape in early-onset prostate cancer

Weischenfeldt, J.; Simon, R.; Feuerbach, L.; Schlangen, K.; Weichenhan, D.; Minner, S.; Wuttig, D.; Warnatz, H. J.; Stehr, H.; Rausch, T.; Jager, N.; Gu, L.; Bogatyrova, O.; Stutz, A. M.; Claus, R.; Eils, J.; Eils, R.; Gerhauser, C.; Huang, P. H.; Hutter, B.; Kabbe, R.; Lawerenz, C.; Radomski, S.; Bartholomae, C. C.; Falth, M.; Gade, S.; Schmidt, M.; Amschler, N.; Hass, T.; Galal, R.; Gjoni, J.; Kuner, R.; Baer, C.; Masser, S.; von Kalle, C.; Zichner, T.; Benes, V.; Raeder, B.; Mader, M.; Amstislavskiy, V.; Avci, M.; Lehrach, H.; Parkhomchuk, D.; Sultan, M.; Burkhardt, L.; Graefen, M.; Huland, H.; Kluth, M.; Krohn, A.; Sirma, H.; Stumm, L.; Steurer, S.; Grupp, K.; Sultmann, H.; Sauter, G.; Plass, C.; Brors, B.; Yaspo Lehrach, Marie L.; Korbel, J. O.; Schlomm, T.

doi:S1535-6108(13)00004-4 [pii]10.1016/j.ccr.2013.01.002

Item

ITEM ACTIONSEXPORT

Add to Basket

Local TagsRelease HistoryDetailsSummary

Released

Journal Article

Integrative genomic analyses reveal an androgen-driven somatic alteration landscape in early-onset prostate cancer

MPS-Authors

Schlangen, K.
Department of Biomedical Optics, Max Planck Institute for Medical Research, Max Planck Society;

/persons/resource/persons95854

Warnatz, H. J.
Department of Biomedical Optics, Max Planck Institute for Medical Research, Max Planck Society;

/persons/resource/persons50570

Stehr, H.
Independent Junior Research Groups (OWL), Max Planck Institute for Molecular Genetics, Max Planck Society;

/persons/resource/persons50066

Amstislavskiy, V.
Human Chromosome 21 (Marie-Laure Yaspo), Dept. of Vertebrate Genomics (Head: Hans Lehrach), Max Planck Institute for Molecular Genetics, Max Planck Society;

/persons/resource/persons50409

Lehrach, H.
Dept. of Vertebrate Genomics (Head: Hans Lehrach), Max Planck Institute for Molecular Genetics, Max Planck Society;

/persons/resource/persons50461

Parkhomchuk, D.
Dept. of Vertebrate Genomics (Head: Hans Lehrach), Max Planck Institute for Molecular Genetics, Max Planck Society;

/persons/resource/persons50584

Sultan, M.
Human Chromosome 21 (Marie-Laure Yaspo), Dept. of Vertebrate Genomics (Head: Hans Lehrach), Max Planck Institute for Molecular Genetics, Max Planck Society;

/persons/resource/persons50655

Yaspo Lehrach, Marie L.
Human Chromosome 21 (Marie-Laure Yaspo), Dept. of Vertebrate Genomics (Head: Hans Lehrach), Max Planck Institute for Molecular Genetics, Max Planck Society;

External Resource

No external resources are shared

Fulltext (restricted access)

There are currently no full texts shared for your IP range.

Fulltext (public)

Weischenfeldt.pdf
(Publisher version), 2MB

Supplementary Material (public)

There is no public supplementary material available

Citation

Weischenfeldt, J., Simon, R., Feuerbach, L., Schlangen, K., Weichenhan, D., Minner, S., et al. (2013). Integrative genomic analyses reveal an androgen-driven somatic alteration landscape in early-onset prostate cancer. Cancer Cell, 23(2), 159-70. doi:S1535-6108(13)00004-4 [pii]10.1016/j.ccr.2013.01.002.

Cite as: https://hdl.handle.net/11858/00-001M-0000-0018-F403-0

Abstract

Early-onset prostate cancer (EO-PCA) represents the earliest clinical manifestation of prostate cancer. To compare the genomic alteration landscapes of EO-PCA with "classical" (elderly-onset) PCA, we performed deep sequencing-based genomics analyses in 11 tumors diagnosed at young age, and pursued comparative assessments with seven elderly-onset PCA genomes. Remarkable age-related differences in structural rearrangement (SR) formation became evident, suggesting distinct disease pathomechanisms. Whereas EO-PCAs harbored a prevalence of balanced SRs, with a specific abundance of androgen-regulated ETS gene fusions including TMPRSS2:ERG, elderly-onset PCAs displayed primarily non-androgen-associated SRs. Data from a validation cohort of > 10,000 patients showed age-dependent androgen receptor levels and a prevalence of SRs affecting androgen-regulated genes, further substantiating the activity of a characteristic "androgen-type" pathomechanism in EO-PCA.