ArticleeLife2015
SPOP mutation leads to genomic instability in prostate cancer.
Article in eLife, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 127 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
127 citing papers in PubMed, 1 synthesis or guideline pooled it, 192 citations in OpenAlex.
- PARP Inhibition in Prostate Cancer With Homologous Recombination Repair Alterations.JCO precision oncology · 2021Pooled it
- Genomics of lethal prostate cancer at diagnosis and castration resistance.The Journal of clinical investigation · 2020Trial
- SPOP-mediated nuclear ubiquitination degradation of p62/SQSTM1 contributes to HR repair.Oncogene · 2026Article
- Divergent roles of SPOP and CHD1 in ACSL4 regulation reveal context-dependent vulnerabilities for targeting ferroptosis.Nature communications · 2026Article
- Prime, trap, and fail: engineering chromatin to potentiate topoisomerase II poisons in prostate cancer.Translational andrology and urology · 2026Article
- Functional dissection ofProceedings of the National Academy of Sciences of the United States of America · 2026Article
- Molecular insights for the tumor suppressor role of SPOP in prostate cancer.Biochimica et biophysica acta. Reviews on cancer · 2026Review
- Review
- Overexpression of the ERG oncogene in prostate cancer identifies candidates for PARP inhibitor-based radiosensitization.The Journal of clinical investigation · 2026Article
- Homologous recombination deficiency and genomic alterations in advanced prostate cancer: insights for precision therapy.The oncologist · 2026Article
- The proteostasis paradox: from systemic collapse in aging to pathway-specific addiction in prostate cancer.Frontiers in cell and developmental biology · 2026Review
- Comparative genomics of an Antarctic sea-ice diatom (Frontiers in microbiology · 2026Article
- Genetic evidence for PARP1 trapping as a driver of PARP inhibitor efficacy in BRCA mutant cancer cells.Nucleic acids research · 2025Article
- Germline-Somatic Liaison Dictates Cancer Subtypes via de novo Steroid Biosynthesis.Cancer discovery · 2025Article
- Systems biology successes and areas for opportunity in prostate cancer.Endocrine-related cancer · 2025Review
- Targeting DNA Damage Response-Mediated Resistance in Non-Small Cell Lung Cancer: From Mechanistic Insights to Drug Development.Current oncology (Toronto, Ont.) · 2025Review
- The Germline and Somatic Origins of Prostate Cancer Heterogeneity.Cancer discovery · 2025Article
- Cul3 substrate adaptor SPOP targets Nup153 for degradation.Molecular biology of the cell · 2025Article
- Trastuzumab and pertuzumab plus carboplatin-based neoadjuvant therapy for HER2-positive breast cancer: a prospective cohort study with integrated genomic and transcriptomic biomarker analysis.Therapeutic advances in medical oncology · 2025Article
- CRISPR/Cas9 Technology Providing the Therapeutic Landscape of Metastatic Prostate Cancer.Pharmaceuticals (Basel, Switzerland) · 2024Review
67 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
Authors and funding
20 authors at 4 institutions in 3 countries.
Funding
Abstract
Genomic instability is a fundamental feature of human cancer often resulting from impaired genome maintenance. In prostate cancer, structural genomic rearrangements are a common mechanism driving tumorigenesis. However, somatic alterations predisposing to chromosomal rearrangements in prostate cancer remain largely undefined. Here, we show that SPOP, the most commonly mutated gene in primary prostate cancer modulates DNA double strand break (DSB) repair, and that SPOP mutation is associated with genomic instability. In vivo, SPOP mutation results in a transcriptional response consistent with BRCA1 inactivation resulting in impaired homology-directed repair (HDR) of DSB. Furthermore, we found that SPOP mutation sensitizes to DNA damaging therapeutic agents such as PARP inhibitors. These results implicate SPOP as a novel participant in DSB repair, suggest that SPOP mutation drives prostate tumorigenesis in part through genomic instability, and indicate that mutant SPOP may increase response to DNA-damaging therapeutics.
Indexed as
Identifiers
What OpenQuestion holds
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.