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Molecular Evolution of Early-Onset Prostate Cancer Identifies Molecular Risk Markers and Clinical Trajectories

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  3. Integrative Genomic Analyses Reveal an Androgen-Driven Somatic Alteration Landscape in Early-Onset Prostate Cancer

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  • Clarissa Gerhauser
  • Francesco Favero
  • Thomas Risch
  • Ronald Simon
  • Lars Feuerbach
  • Yassen Assenov
  • Doreen Heckmann
  • Nikos Sidiropoulos
  • Sebastian M Waszak
  • Daniel Hübschmann
  • Alfonso Urbanucci
  • Etsehiwot G Girma
  • Vladimir Kuryshev
  • Leszek J Klimczak
  • Natalie Saini
  • Adrian M Stütz
  • Dieter Weichenhan
  • Lisa-Marie Böttcher
  • Reka Toth
  • Josephine D Hendriksen
  • Christina Koop
  • Pavlo Lutsik
  • Sören Matzk
  • Hans-Jörg Warnatz
  • Vyacheslav Amstislavskiy
  • Clarissa Feuerstein
  • Benjamin Raeder
  • Olga Bogatyrova
  • Eva-Maria Schmitz
  • Claudia Hube-Magg
  • Martina Kluth
  • Hartwig Huland
  • Markus Graefen
  • Chris Lawerenz
  • Gervaise H Henry
  • Takafumi N Yamaguchi
  • Alicia Malewska
  • Jan Meiners
  • Daniela Schilling
  • Eva Reisinger
  • Roland Eils
  • Matthias Schlesner
  • Douglas W Strand
  • Robert G Bristow
  • Paul C Boutros
  • Christof von Kalle
  • Dmitry Gordenin
  • Holger Sültmann
  • Benedikt Brors
  • Guido Sauter
  • Christoph Plass
  • Marie-Laure Yaspo
  • Jan O Korbel
  • Thorsten Schlomm
  • Joachim Weischenfeldt
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Identifying the earliest somatic changes in prostate cancer can give important insights into tumor evolution and aids in stratifying high- from low-risk disease. We integrated whole genome, transcriptome and methylome analysis of early-onset prostate cancers (diagnosis ≤55 years). Characterization across 292 prostate cancer genomes revealed age-related genomic alterations and a clock-like enzymatic-driven mutational process contributing to the earliest mutations in prostate cancer patients. Our integrative analysis identified four molecular subgroups, including a particularly aggressive subgroup with recurrent duplications associated with increased expression of ESRP1, which we validate in 12,000 tissue microarray tumors. Finally, we combined the patterns of molecular co-occurrence and risk-based subgroup information to deconvolve the molecular and clinical trajectories of prostate cancer from single patient samples.

Original languageEnglish
JournalCancer Cell
Volume34
Issue number6
Pages (from-to)996-1011.e8
ISSN1535-6108
DOIs
Publication statusPublished - 10 Dec 2018

ID: 55804759