ArticlePLoS genetics2017
Appraising the relevance of DNA copy number loss and gain in prostate cancer using whole genome DNA sequence data.
Article in PLoS genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
30 citing papers in PubMed, 43 citations in OpenAlex.
- RNASEH2B loss and PARP inhibition in advanced prostate cancer.The Journal of clinical investigation · 2024Trial
- Recurrent mechanisms of biallelic epigenetic inactivation reveal new putative tumour suppressor genes in prostate cancer.Nature communications · 2026Article
- Article
- Mechanisms of Progression and Challenges for Intervention in the Natural History of Early Prostate Cancer: A Narrative Review.Current oncology (Toronto, Ont.) · 2026Review
- Deletions ofBiomolecules · 2025Article
- Racial disparity in prostate cancer: an outlook in genetic and molecular landscape.Cancer metastasis reviews · 2024Review
- Prostate Cancer Progression Modeling Provides Insight into Dynamic Molecular Changes Associated with Progressive Disease States.Cancer research communications · 2024Article
- The yin and yang of chromosomal instability in prostate cancer.Nature reviews. Urology · 2024Review
- Androgen receptor and MYC transcriptomes are equilibrated in multilayer regulatory circuitries in prostate cancer.The Prostate · 2023Article
- Dissecting transcription of the 8q24-MYC locus in prostate cancer recognizes the equilibration between androgen receptor direct and indirect dual-functions.Journal of translational medicine · 2023Article
- Chromosome-specific segment size alterations are determinants of prognosis in prostate cancer.Saudi journal of biological sciences · 2023Article
- Systematic integration of protein-affecting mutations, gene fusions, and copy number alterations into a comprehensive somatic mutational profile.Cell reports methods · 2023Article
- Article
- The architecture of clonal expansions in morphologically normal tissue from cancerous and non-cancerous prostates.Molecular cancer · 2022Article
- Study on the Mechanism of circRNA-0024103 Reducing Endothelial Cell Injury by Regulating miR-363/MMP-10.Contrast media & molecular imaging · 2022Article
- Convergent evolution of a genomic rearrangement may explain cancer resistance in hystrico- and sciuromorpha rodents.NPJ aging and mechanisms of disease · 2021Article
- Combining targeted sequencing and ultra-low-pass whole-genome sequencing for accurate somatic copy number alteration detection.Functional & integrative genomics · 2021Article
- Are Molecular Alterations Linked to Genetic Instability Worth to Be Included as Biomarkers for Directing or Excluding Melanoma Patients to Immunotherapy?Frontiers in oncology · 2021Review
- Observational
- Exome sequencing identified six copy number variations as a prediction model for recurrence of primary prostate cancers with distinctive prognosis.Translational cancer research · 2020Article
Corrections and comments
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Authors and funding
57 authors at 16 institutions in 5 countries.
Funding
Abstract
A variety of models have been proposed to explain regions of recurrent somatic copy number alteration (SCNA) in human cancer. Our study employs Whole Genome DNA Sequence (WGS) data from tumor samples (n = 103) to comprehensively assess the role of the Knudson two hit genetic model in SCNA generation in prostate cancer. 64 recurrent regions of loss and gain were detected, of which 28 were novel, including regions of loss with more than 15% frequency at Chr4p15.2-p15.1 (15.53%), Chr6q27 (16.50%) and Chr18q12.3 (17.48%). Comprehensive mutation screens of genes, lincRNA encoding sequences, control regions and conserved domains within SCNAs demonstrated that a two-hit genetic model was supported in only a minor proportion of recurrent SCNA losses examined (15/40). We found that recurrent breakpoints and regions of inversion often occur within Knudson model SCNAs, leading to the identification of ZNF292 as a target gene for the deletion at 6q14.3-q15 and NKX3.1 as a two-hit target at 8p21.3-p21.2. The importance of alterations of lincRNA sequences was illustrated by the identification of a novel mutational hotspot at the KCCAT42, FENDRR, CAT1886 and STCAT2 loci at the 16q23.1-q24.3 loss. Our data confirm that the burden of SCNAs is predictive of biochemical recurrence, define nine individual regions that are associated with relapse, and highlight the possible importance of ion channel and G-protein coupled-receptor (GPCR) pathways in cancer development. We concluded that a two-hit genetic model accounts for about one third of SCNA indicating that mechanisms, such haploinsufficiency and epigenetic inactivation, account for the remaining SCNA losses.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.