Inherited determinants of early recurrent somatic mutations in prostate cancer
Open accessAbstract
Prostate cancer is a highly heritable molecularly and clinically heterogeneous disease. To discover germline events involved in prostate cancer predisposition, we develop a computational approach to nominate heritable facilitators of somatic genomic events in the context of the androgen receptor signaling. Here, we use a ranking score and benign prostate transcriptomes to identify a non-coding polymorphic regulatory element at 7p14.3 that associates with DNA repair and hormone-regulated transcript levels and with an early recurrent prostate cancer-specific somatic mutation in the Speckle-Type POZ protein (SPOP) gene. The locus shows allele-specific activity that is concomitantly modulated by androgen receptor and by CCAAT/enhancer-binding protein (C/EBP) beta (CEBPB). Deletion of this locus via CRISPR-Cas9 leads to deregulation of the genes predicted to interact with the 7p14.3 locus by Hi-C chromosome conformation capture data. This study suggests that a polymorphism at 7p14.3 may predispose to SPOP mutant prostate cancer subclass through a hormone-dependent DNA damage response.
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CRISPR-nucleases have been successfully used to induce NHEJ to knockout genes or genomic regulatory elements, including permanent repair of splicing defects in CFTR minigene models.
“CRISPR-nucleases have been successfully used to induce NHEJ to knockout genes or genomic regulatory elements25,26. This includes permanent repair of splicing defects in CFTR minigene models27 as an alternative to the transient and inefficient use of oligonucleotides or spliceosome-mediated RNA trans-splicing (SMaRT) strategies28,29.”
From Allele specific repair of splicing mutations in cystic fibrosis through AsCas12a genome editing (2019) · cites this paper as [25]
Citation 27 is attached to the claim about permanent repair of CFTR splicing defects. The Methods section, “CRISPR-Cas9 7p14.3 deleted locus in PC-3 cells” (page unavailable), describes deletion of a prostate-cell genomic locus, not a CFTR minigene. Searches for CFTR minigene repair and splicing defects found no passage addressing that claim. (LLM, conf=0.72)
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- Authors
- Romanel, A., Garritano, S., Stringa, B., Blattner, M., Dalfovo, D., Chakravarty, D., Soong, D., Cotter, K. A., Petris, G., Dhingra, P., Gasperini, P., Cereseto, A., Elemento, O., Sboner, A., Khurana, E., Inga, A., Rubin, M. A., & Demichelis, F.
- Affiliations
- University of Trento (IT)
- NewYork–Presbyterian Hospital (US)
- Weill Cornell Medicine (US)
- Corresponding author
- Demichelis, Francesca
- ORCID
- Venue
- Nature Communications
- Published
- 2017-06-29
- Volume
- 8
- Issue
- 1
- Pages
- 48-48
- ISSN
- 2041-1723 (ISSN-L)
- PMC
- PMC5491529
- OpenAlex
- W2701391316
- Cited by
- 29
- References
- 44
- Citations by year
- 2025: 3 · 2024: 3 · 2023: 3 · 2022: 4 · 2021: 3 · 2020: 3 · 2019: 5 · 2018: 4 · 2017: 1
- FWCI
- 2.94
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Nature Communications (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Institutional Research Information System (University of Udine) (submittedVersion)
- Bern Open Repository and Information System (University of Bern) (submittedVersion, cc-by)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Iris (University of Trento) (submittedVersion, other-oa)
- Open Access CRIS of the University of Bern
- Funders
- U.S. Department of Defense
- Università degli Studi di Trento
- Associazione Italiana per la Ricerca sul Cancro
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Prostate Cancer Treatment and Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Chromatin Remodeling and Cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
- Keywords
- prostate cancer, SPOP, somatic mutations, germline predisposition, non-coding polymorphisms, regulatory elements, androgen receptor signaling, C/EBPβ, DNA repair, DNA damage response, allele-specific expression, CRISPR/Cas9 gene deletion, chromosome conformation
- MeSH terms
- Genotype, Humans, Male, Mutation, Neoplasm Recurrence, Local, Prostatic Neoplasms, Gene Expression Regulation, Neoplastic, Cell Line, Tumor, Transcriptome
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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