A recurrent truncating germline mutation in the BRIP1/FANCJ gene and susceptibility to prostate cancer
Open accessAbstract
Although prostate cancer (PrCa) is one of the most common cancers in men in Western countries, little is known about the inherited factors that influence PrCa risk. On the basis of the fact that BRIP1/FANCJ interacts with BRCA1 and functions as a regulator of DNA double-strand break repair pathways, and that germline mutations within the BRIP1/FANCJ gene predispose to breast cancer, we chose this gene as a candidate for mutation screening in familial and young-onset PrCa cases. We identified a truncating mutation, R798X, in the BRIP1/FANCJ gene in 4 out of 2714 UK PrCa cases enriched for familial (2 out of 641; 0.3%) and young-onset cases (2 out of 2073; 0.1%). On screening 2045 controls from the UK population, we found one R798X sequence alteration (0.05%; odds ratio 2.4 (95% CI 0.25-23.4)). In addition, using our data from a genome-wide association study, we analysed 25 SNPs in the genomic region of the BRIP1/FANCJ gene. Two SNPs showed evidence of association with familial and young-onset PrCa (rs6504074; P(trend)=0.04 and rs8076727; P(trend)=0.01). These results suggest that truncating mutations in BRIP1/FANCJ might confer an increased risk of PrCa and common SNPs might also contribute to the alteration of risk, but larger case-control series will be required to confirm or refute this association.
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The most common FANCJ germline mutant allele is R798x.
“Of all the FANCJ germline mutations, the most common mutant allele is FANCJ R798x.”
From Hereditary Breast Cancer and the BRCA1-Associated FANCJ/BACH1/BRIP1 (2011) · cites this paper as [58]
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- Authors
- The UKGPCS Collaborators, T. B. A. O. U. S. S. O. O., Kote-Jarai, Z., Jugurnauth, S., Mulholland, S., Leongamornlert, D. A., Guy, M., Edwards, S., Tymrakiewitcz, M., O'Brien, L., Hall, A., Wilkinson, R., Al Olama, A. A., Morrison, J., Muir, K., Neal, D., Donovan, J., Hamdy, F., Easton, D. F., & Eeles, R.
- Affiliations
- Institute of Cancer Research (GB)
- Royal Marsden NHS Foundation Trust (GB)
- University of Cambridge (GB)
- University of Nottingham (GB)
- University of Bristol (GB)
- University of Sheffield (GB)
- Corresponding author
- Eeles, R
- Venue
- British Journal of Cancer
- Published
- 2009-01
- Volume
- 100
- Issue
- 2
- Pages
- 426-430
- ISSN
- 0007-0920 (ISSN-L)
- 1532-1827
- PMC
- PMC2634720
- OpenAlex
- W2005299967
- Cited by
- 91
- References
- 18
- Citations by year
- 2026: 4 · 2025: 5 · 2024: 2 · 2023: 29 · 2022: 1 · 2021: 5 · 2020: 7 · 2019: 3 · 2018: 7 · 2017: 3 · 2016: 1 · 2015: 7 · 2014: 3 · 2013: 4 · 2012: 4
- FWCI
- 1.94
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- cc-by-nc-sa
- www.springer.com/tdm (unspecified)
- Locations
- British Journal of Cancer (publishedVersion, cc-by-nc-sa)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Explore Bristol Research (submittedVersion)
- Funders
- Cancer Research Institute
- National Cancer Research Institute
- Cancer Research UK (C5047/A3354, C522/A8649, 10118, 11022)
- National Institute for Health and Care Research (96/20/99)
- Health Technology Assessment Programme (96/20/99, 96/20/06, 96/20/99, 96/20/06)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › BRCA gene mutations in cancer
- Health Sciences › Medicine › Pathology and Forensic Medicine › Genetic factors in colorectal cancer
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Prostate Cancer Treatment and Research
- Keywords
- prostate cancer, germline mutations, truncating mutations, hereditary cancer predisposition, familial prostate cancer, single nucleotide polymorphisms, DNA double-strand break repair, cancer susceptibility
- MeSH terms
- Aged, DNA, DNA-Binding Proteins, Female, Humans, Male, Middle Aged, Pedigree, Prognosis, Prostatic Neoplasms, Case-Control Studies, Age of Onset, Germ-Line Mutation, Genetic Predisposition to Disease, RNA Helicases, Polymorphism, Single Nucleotide, Fanconi Anemia Complementation Group Proteins, Genome-Wide Association Study
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