BRCA1, BRCA2, PALB2, and CDKN2A mutations in familial pancreatic cancer: a PACGENE study
Open accessAbstract
Purpose Familial pancreatic cancer kindreds contain at least two affected first-degree relatives. Comprehensive data are needed to assist clinical risk assessment and genetic testing.Methods Germ-line DNA samples from 727 unrelated probands with positive family history (521 met criteria for familial pancreatic cancer) were tested in compliance with the Clinical Laboratory Improvement Amendments for mutations in BRCA1 and BRCA2 (including analysis of deletions and rearrangements), PALB2, and CDKN2A. We compared prevalence of deleterious mutations between familial pancreatic cancer probands and nonfamilial pancreatic cancer probands (kindreds containing at least two affected biological relatives, but not first-degree relatives). We also examined the impact of family history on breast and ovarian cancers and melanoma.Results Prevalence of deleterious mutations (excluding variants of unknown significance) among familial pancreatic cancer probands was: BRCA1, 1.2%; BRCA2, 3.7%; PALB2, 0.6%; and CDKN2A, 2.5%. Four novel deleterious mutations were detected. Familial pancreatic cancer probands carry more mutations in the four genes (8.0%) than nonfamilial pancreatic cancer probands (3.5%) (odds ratio: 2.40; 95% confidence interval: 1.06-5.44; P = 0.03). The probability of testing positive for deleterious mutations in any of the four genes ranges up to 10.4%, depending on family history of cancers. BRCA2 and CDKN2A account for the majority of mutations in familial pancreatic cancer.Conclusion Genetic testing of multiple relevant genes in probands with a positive family history is warranted, particularly for familial pancreatic cancer.
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In familial pancreatic cancer (FPC), CDKN2A mutations, along with BRCA2 and PALB2, were prevalent, particularly in FPC probands.
“In familial pancreatic cancer (FPC), CDKN2A mutations, along with those in BRCA2 and PALB2, were prevalent, particularly in FPC probands, highlighting their significance in hereditary pancreatic cancer [43].”
From Significance of TP53, CDKN2A, SMAD4 and KRAS in Pancreatic Cancer (2024) · cites this paper as [43]
The Results (page unavailable) report that deleterious mutations in the four genes were more common collectively in FPC probands than in familial non-FPC probands (8.0% versus 3.5%). They also state that BRCA2 and CDKN2A mutations were more prevalent than PALB2 mutations, so describing all three as similarly prevalent overstates the finding. The Discussion (page unavailable) reports no significant FPC-versus-non-FPC difference for BRCA2 individually. (LLM, conf=0.86)
Experimental — accuracy not yet measuredApproximately 5-7% of PDAC patients harbor a germline mutation in a Fanconi anemia family gene (BRCA1, BRCA2, PALB2) involved in homologous recombination repair.
“Approximately 5–7% of patients with PDAC harbor a germline mutation in one of the Fanconi anemia family of genes (BRCA1, BRCA2, and PALB2) encoding for proteins engaged in homologous recombination repair85.”
From Pancreatic cancer: Advances and challenges (2023) · cites this paper as [85]
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- Authors
- Zhen, D. B., Rabe, K. G., Gallinger, S., Syngal, S., Schwartz, A. G., Goggins, M. G., Hruban, R. H., Cote, M. L., McWilliams, R. R., Roberts, N. J., Cannon-Albright, L. A., Li, D., Moyes, K., Wenstrup, R. J., Hartman, A.-R., Seminara, D., Klein, A. P., & Petersen, G. M.
- Affiliations
- Mayo Clinic (US)
- Brigham and Women's Hospital (US)
- Wayne State University (US)
- Johns Hopkins University (US)
- The University of Texas MD Anderson Cancer Center (US)
- Myriad Genetics (US)
- National Cancer Institute (US)
- Corresponding author
- Petersen, Gloria M.
- ORCID
- Venue
- Genetics in Medicine
- Publisher
- Elsevier BV
- Published
- 2015-07
- Volume
- 17
- Issue
- 7
- Pages
- 569-577
- ISSN
- 1098-3600 (ISSN-L)
- PMC
- PMC4439391
- OpenAlex
- W2092259915
- Cited by
- 295
- References
- 39
- Citations by year
- 2026: 13 · 2025: 13 · 2024: 26 · 2023: 26 · 2022: 27 · 2021: 39 · 2020: 30 · 2019: 29 · 2018: 34 · 2017: 21 · 2016: 25 · 2015: 12
- FWCI
- 12.66
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Genetics in Medicine (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- American Association for Cancer Research
- University of Utah
- Johns Hopkins University
- Myriad Genetics
- National Institutes of Health (N01-PC35145, n01pc35145-19-0-7, PC35145, CA62924, CA102701)
- National Cancer Institute (P30CA 22453, CA102701, R01CA-97075, CA-22453, N01 PC035145, P50CA-62924, N01 PC 35145, P50CA102701, R01CA090709, R01CA097075, P50CA062924, P30CA015083, P30CA022453, P30CA006973, CA 62924)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › BRCA gene mutations in cancer
- Health Sciences › Medicine › Oncology › Pancreatic and Hepatic Oncology Research
- Health Sciences › Medicine › Pathology and Forensic Medicine › Genetic factors in colorectal cancer
- Keywords
- familial pancreatic cancer, BRCA1, BRCA2, PALB2, CDKN2A, germline mutations, deleterious mutations, mutation prevalence, genetic testing, family history (medicine), breast cancer, ovarian cancer, melanoma, novel mutations
- MeSH terms
- Fanconi Anemia Complementation Group N Protein, Adult, Aged, Aged, 80 and over, Carcinoma, Female, Humans, Male, Middle Aged, Nuclear Proteins, Pancreatic Neoplasms, Germ-Line Mutation, Genes, BRCA1, Cyclin-Dependent Kinase Inhibitor p16, Genes, p16, Genetic Predisposition to Disease, Genes, BRCA2, BRCA2 Protein, Tumor Suppressor Proteins, Ubiquitin-Protein Ligases
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