ArticleNeoplasia (New York, N.Y.)2014
SPOP mutations in prostate cancer across demographically diverse patient cohorts.
Article in Neoplasia (New York, N.Y.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 papers, 1 of them a synthesis that pooled it.
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Who cites it
106 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Prevalence and clinical application ofAsian journal of andrologyPooled it
- Mapping prostate cancer pathobiology: A review of genetically engineered mouse models (GEMMs).Gene · 2026Review
- MYC contributes to targeted therapy resistance in lung cancers driven by MET exon 14-skipping alteration.NPJ precision oncology · 2026Article
- Review
- Genomic landscape and precision therapy in prostate cancer: current status and future directions.NPJ precision oncology · 2026Review
- Systematic Characterization of Cancer-Associated SPOP Mutants Reveals Novel and Reprogrammable Degradative Activities.Chembiochem : a European journal of chemical biology · 2026Article
- Precision Medicine in Prostate Cancer with a Focus on Emerging Therapeutic Strategies.Biomedicines · 2025Review
- Prevalence of SPOP and IDH Gene Mutations in Prostate Cancer in a Jordanian Population.Biochemical genetics · 2025Article
- Deep Sequencing Reveals Novel Mutations inInternational journal of molecular sciences · 2025Article
- Scaling for African Inclusion in High-Throughput Whole Cancer Genome Bioinformatic Workflows.Cancers · 2025Review
- Review
- Challenges and opportunities for the diverse substrates of SPOP E3 ubiquitin ligase in cancer.Theranostics · 2025Review
- Updates on SPOP Gene Mutations in Prostate Cancer and Computational Insights From TCGA cBioPortal Database.Scientifica · 2025Review
- The tripartite motif-containing 24 is a multifunctional player in human cancer.Cell & bioscience · 2024Review
- Review
- Interrogating bromodomain inhibitor resistance in KMT2A-rearranged leukemia through combinatorial CRISPR screens.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- The Prevalence of CHEK1 and CHEK2 Mutations in Prostate Cancer: a Retrospective Cohort Study.Medical archives (Sarajevo, Bosnia and Herzegovina) · 2023Article
- GENOMICS OF PROSTATE CANCER: CLINICAL UTILITY AND CHALLENGES.Acta clinica Croatica · 2022Review
- Race and prostate cancer: genomic landscape.Nature reviews. Urology · 2022Review
- Developing New Treatment Options for Castration-Resistant Prostate Cancer and Recurrent Disease.Biomedicines · 2022Review
46 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
26 authors.
Funding
Abstract
backgroundRecurrent mutations in the Speckle-Type POZ Protein (SPOP) gene occur in up to 15% of prostate cancers. However, the frequency and features of cancers with these mutations across different populations is unknown.
objectiveTo investigate SPOP mutations across diverse cohorts and validate a series of assays employing high-resolution melting (HRM) analysis and Sanger sequencing for mutational analysis of formalin-fixed paraffin-embedded material. DESIGN SETTING AND
participants720 prostate cancer samples from six international cohorts spanning Caucasian, African American, and Asian patients, including both prostate-specific antigen-screened and unscreened populations, were screened for their SPOP mutation status. Status of SPOP was correlated to molecular features (ERG rearrangement, PTEN deletion, and CHD1 deletion) as well as clinical and pathologic features. RESULTS AND LIMITATIONS: Overall frequency of SPOP mutations was 8.1% (4.6% to 14.4%), SPOP mutation was inversely associated with ERG rearrangement (P<.01), and SPOP mutant (SPOPmut) cancers had higher rates of CHD1 deletions (P<.01). There were no significant differences in biochemical recurrence in SPOPmut cancers. Limitations of this study include missing mutational data due to sample quality and lack of power to identify a difference in clinical outcomes.
conclusionSPOP is mutated in 4.6% to 14.4% of patients with prostate cancer across different ethnic and demographic backgrounds. There was no significant association between SPOP mutations with ethnicity, clinical, or pathologic parameters. Mutual exclusivity of SPOP mutation with ERG rearrangement as well as a high association with CHD1 deletion reinforces SPOP mutation as defining a distinct molecular subclass of prostate cancer.
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