ArticleNature communications2017
Inherited determinants of early recurrent somatic mutations in prostate cancer.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 30 citations in OpenAlex.
- CEBPB emerges as a key regulatory factor in human cancers through diverse molecular mechanisms and clinical implications.Discover oncology · 2025Review
- Germline-Somatic Liaison Dictates Cancer Subtypes via de novo Steroid Biosynthesis.Cancer discovery · 2025Article
- The Germline and Somatic Origins of Prostate Cancer Heterogeneity.Cancer discovery · 2025Article
- Lipopeptide-mediated Cas9 RNP delivery: A promising broad therapeutic strategy for safely removing deep-intronic variants inMolecular therapy. Nucleic acids · 2024Article
- Treatment escalation and de-escalation of de-novo metastatic castration-sensitive prostate cancer.Nagoya journal of medical science · 2024Review
- Germline determinants of aberrant signaling pathways in cancer.NPJ precision oncology · 2024Article
- Identification and validation of cancer-associated fibroblast-related subtypes and the prognosis model of biochemical recurrence in prostate cancer based on single-cell and bulk RNA sequencing.Journal of cancer research and clinical oncology · 2023Article
- A polygenic two-hit hypothesis for prostate cancer.Journal of the National Cancer Institute · 2023Article
- Review
- Article
- Polympact: exploring functional relations among common human genetic variants.Nucleic acids research · 2022Article
- Article
- Molecular medicine tumor board: whole-genome sequencing to inform on personalized medicine for a man with advanced prostate cancer.Prostate cancer and prostatic diseases · 2021Article
- The diverse roles of SPOP in prostate cancer and kidney cancer.Nature reviews. Urology · 2020Review
- The emerging role of SPOP protein in tumorigenesis and cancer therapy.Molecular cancer · 2020Review
- Allele specific repair of splicing mutations in cystic fibrosis through AsCas12a genome editing.Nature communications · 2019Article
- Dysregulated Transcriptional Control in Prostate Cancer.International journal of molecular sciences · 2019Review
- Mapping the Germline and Somatic Mutation Interaction Landscape in Indolent and Aggressive Prostate Cancers.Journal of oncology · 2019Article
- VSV-G-Enveloped Vesicles for Traceless Delivery of CRISPR-Cas9.Molecular therapy. Nucleic acids · 2018Article
- Prostate Cancer Genomics: Recent Advances and the Prevailing Underrepresentation from Racial and Ethnic Minorities.International journal of molecular sciences · 2018Review
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Authors and funding
18 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.Prostate cancer is a heterogeneous disease, and many cases show somatic mutations of SPOP. Here, the authors show that a non-coding polymorphic regulatory element at 7p14.3 may predispose to SPOP mutant prostate cancer subclass through a hormone dependent DNA damage response.
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