ArticleThe Prostate2014
Identification of a novel germline SPOP mutation in a family with hereditary prostate cancer.
Article in The Prostate, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 21 citations in OpenAlex.
- Article
- Article
- Review
- The diverse roles of SPOP in prostate cancer and kidney cancer.Nature reviews. Urology · 2020Review
- SPOP and cancer: a systematic review.American journal of cancer research · 2020Review
- Familial/inherited cancer syndrome: a focus on the highly consanguineous Arab population.NPJ genomic medicine · 2020Review
- Differential Expression of Genes for Ubiquitin Ligases in Medulloblastoma Subtypes.Cerebellum (London, England) · 2019Article
- Identification of novel sarcoma risk genes using a two-stage genome wide DNA sequencing strategy in cancer cluster families and population case and control cohorts.BMC medical genetics · 2019Article
- Hedgehog Signal and Genetic Disorders.Frontiers in genetics · 2019Review
- Functional analysis of Cullin 3 E3 ligases in tumorigenesis.Biochimica et biophysica acta. Reviews on cancer · 2018Review
- Somatic Mutations in Prostate Cancer: Closer to Personalized Medicine.Molecular diagnosis & therapy · 2017Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundFamily history of prostate cancer is a well-recognized risk factor. Previous linkage studies have reported a putative prostate cancer susceptibility locus at chromosome 17q21-22. SPOP (Speckle-type POZ protein) maps to the 17q21-22 candidate linkage region and is one of the most frequently mutated genes in sporadic prostate cancers.
methodsWe performed targeted next generation sequencing to analyze 2009 exons from 202 genes in a candidate linkage region on chromosome 17q21-22 using 94 unrelated familial prostate cancer cases from the University of Michigan Prostate Cancer Genetics Project (n=54) and Johns Hopkins University (n=40) including the exons and UTRs of SPOP.
resultsWe identified a novel SPOP missense mutation (N296I) in a man with prostate cancer diagnosed at age 43. This mutation completely segregates with prostate cancer affection status among the men in this family. The N296I mutation resides within the evolutionarily conserved Bric-a-brac, Tramtrack, Broad-complex (BTB) domain, involved in recruiting targets to Cul3 for degradation. Analysis of the prostate tumor from this individual verified the presence of heterozygous N296I as well as an ERG fusion.
conclusionsWe have discovered a novel mutation in SPOP that tracks with prostate cancer within a family and is predicted to be deleterious. Taken together, our results implicate SPOP as a candidate gene for hereditary prostate cancer.
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