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Gewählte Publikation:

SHR Neuro Krebs Kardio Lipid

Ulz, P; Belic, J; Graf, R; Auer, M; Lafer, I; Fischereder, K; Webersinke, G; Pummer, K; Augustin, H; Pichler, M; Hoefler, G; Bauernhofer, T; Geigl, JB; Heitzer, E; Speicher, MR.
Whole-genome plasma sequencing reveals focal amplifications as a driving force in metastatic prostate cancer.
Nat Commun. 2016; 7(9):12008-12008 [OPEN ACCESS]
Web of Science PubMed PUBMED Central FullText FullText_MUG

 

Autor/innen der Med Uni Graz:
Auer Martina
Augustin Herbert
Bauernhofer Thomas
Belic Jelena
Fischereder Katja
Geigl Jochen Bernd
Graf Ricarda
Heitzer Ellen
Hoefler Gerald
Lafer Ingrid
Pichler Martin
Pummer Karl
Speicher Michael
Ulz Peter
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Number of Figures: 4
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Abstract:
Genomic alterations in metastatic prostate cancer remain incompletely characterized. Here we analyse 493 prostate cancer cases from the TCGA database and perform whole-genome plasma sequencing on 95 plasma samples derived from 43 patients with metastatic prostate cancer. From these samples, we identify established driver aberrations in a cancer-related gene in nearly all cases (97.7%), including driver gene fusions (TMPRSS2:ERG), driver focal deletions (PTEN, RYBP and SHQ1) and driver amplifications (AR and MYC). In serial plasma analyses, we observe changes in focal amplifications in 40% of cases. The mean time interval between new amplifications was 26.4 weeks (range: 5-52 weeks), suggesting that they represent rapid adaptations to selection pressure. An increase in neuron-specific enolase is accompanied by clonal pattern changes in the tumour genome, most consistent with subclonal diversification of the tumour. Our findings suggest a high plasticity of prostate cancer genomes with newly occurring focal amplifications as a driving force in progression.

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