| Literature DB >> 30889379 |
Ankit Sinha1, Vincent Huang2, Julie Livingstone2, Jenny Wang3, Natalie S Fox4, Natalie Kurganovs5, Vladimir Ignatchenko6, Katharina Fritsch7, Nilgun Donmez8, Lawrence E Heisler2, Yu-Jia Shiah2, Cindy Q Yao2, Javier A Alfaro4, Stas Volik8, Anna Lapuk8, Michael Fraser2, Ken Kron6, Alex Murison6, Mathieu Lupien9, Cenk Sahinalp8, Colin C Collins10, Bernard Tetu11, Mehdi Masoomian12, David M Berman13, Theodorus van der Kwast14, Robert G Bristow15, Thomas Kislinger16, Paul C Boutros17.
Abstract
DNA sequencing has identified recurrent mutations that drive the aggressiveness of prostate cancers. Surprisingly, the influence of genomic, epigenomic, and transcriptomic dysregulation on the tumor proteome remains poorly understood. We profiled the genomes, epigenomes, transcriptomes, and proteomes of 76 localized, intermediate-risk prostate cancers. We discovered that the genomic subtypes of prostate cancer converge on five proteomic subtypes, with distinct clinical trajectories. ETS fusions, the most common alteration in prostate tumors, affect different genes and pathways in the proteome and transcriptome. Globally, mRNA abundance changes explain only ∼10% of protein abundance variability. As a result, prognostic biomarkers combining genomic or epigenomic features with proteomic ones significantly outperform biomarkers comprised of a single data type.Entities:
Keywords: biomarker; epigenome; genome; multi-omic features; prostate cancer; proteome; transcriptome
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Year: 2019 PMID： 30889379 PMCID： PMC6511374 DOI： 10.1016/j.ccell.2019.02.005
Source DB: PubMed Journal: Cancer Cell ISSN： 1535-6108 Impact factor: 31.743