Study

Whole-genome plasma sequencing reveals focal amplifications as a driving force in metastatic prostate cancer

Study ID Alternative Stable ID Type
EGAS00001001018 Other

Study Description

Genomic alterations in metastatic prostate cancer remain incompletely characterized. Here we analyze 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, SHQ1), and driver amplifications (AR, 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 tumor genome, most consistent with subclonal diversification of the tumor. Our findings suggest a high plasticity of prostate cancer genomes with newly occurring focal amplifications as a driving force in progression

Study Datasets 2 datasets.

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Dataset ID Description Technology Samples
EGAD00001002149
Low coverage whole genome sequencing for the identification of somatic copy number alterations (SCNA) and focal amplification mapping in plasma DNA of prostate cancer patients
Illumina MiSeq 95
EGAD00001002150
Low coverage whole genome sequencing for the identification of somatic copy number alterations (SCNA) and focal amplification mapping of corresponding tumor material
Illumina MiSeq 8

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