Risk of Pancreatic Cancer in Families With Lynch Syndrome
Open accessAbstract
CONTEXT: Lynch syndrome is an inherited cause of colorectal cancer caused by mutations of DNA mismatch repair (MMR) genes. A number of extracolonic tumors have been associated with the disorder, including pancreatic cancer; however, the risk of pancreatic cancer in Lynch syndrome is uncertain and not quantified. OBJECTIVE: To estimate pancreatic cancer risk in families with germline MMR gene mutations. DESIGN, SETTING, AND PATIENTS: Cancer histories of probands and their relatives were evaluated in MMR gene mutation carriers in the familial cancer registries of the Dana-Farber Cancer Institute (n = 80), Boston, Massachusetts, and University of Michigan Comprehensive Cancer Center (n = 67), Ann Arbor, Michigan. Families enrolled before the study start date (June 2008) were eligible. Age-specific cumulative risks and hazard ratio estimates of pancreatic cancer risk were calculated and compared with the general population using modified segregation analysis, with correction for ascertainment. MAIN OUTCOME MEASURES: Age-specific cumulative risks and hazard ratio estimates of pancreatic cancer risk. RESULTS: Data on 6342 individuals from 147 families with MMR gene mutations were analyzed. Thirty-one families (21.1%) reported at least 1 case of pancreatic cancer. Forty-seven pancreatic cancers were reported (21 men and 26 women), with no sex-related difference in age of diagnosis (51.5 vs 56.5 years for men and women, respectively). The cumulative risk of pancreatic cancer in these families with gene mutations was 1.31% (95% confidence interval [CI], 0.31%-2.32%) up to age 50 years and 3.68% (95% CI, 1.45%-5.88%) up to age 70 years, which represents an 8.6-fold increase (95% CI, 4.7-15.7) compared with the general population. CONCLUSIONS: Among 147 families with germline MMR gene mutations, the risk of pancreatic cancer was increased compared with the US population. Individuals with MMR gene mutations and a family history of pancreatic cancer are appropriate to include in studies to further define the risk of premalignant and malignant pancreatic neoplasms and potential benefits and limitations of surveillance.
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Pancreatic surveillance is recommended for carriers of germline deleterious variants in BRCA2, ATM, BRCA1, PALB2, CDKN2A, STK11, MLH1 and MSH2.
“Pancreatic surveillance is recommended for carriers of germline deleterious variants in cancer susceptibility gene,22–26: BRCA2, ATM, BRCA1, PALB2, CDKN2A, STK11, MLH1 and MSH2.”
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- Authors
- Kastrinos, F.
- Affiliations
- Brigham and Women's Hospital (US)
- Corresponding author
- Kastrinos, Fay
- ORCID
- Kastrinos, Fay
- Venue
- JAMA
- Publisher
- American Medical Association (AMA)
- Published
- 2009-10-28
- Volume
- 302
- Issue
- 16
- Pages
- 1790
- ISSN
- 0002-9955 (ISSN-L)
- 0098-7484
- PMC
- PMC4091624
- OpenAlex
- W1980125751
- Cited by
- 544
- References
- 39
- Citations by year
- 2026: 17 · 2025: 25 · 2024: 29 · 2023: 34 · 2022: 42 · 2021: 38 · 2020: 42 · 2019: 38 · 2018: 44 · 2017: 30 · 2016: 43 · 2015: 38 · 2014: 27 · 2013: 26 · 2012: 33
- FWCI
- 16.20
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- JAMA (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Cancer Institute (R01CA-97075, R01 CA81488, 5P30 CA 46592, K24CA113433, R01CA097075, R01CA081488, P30CA046592)
- Topics
- Health Sciences › Medicine › Pathology and Forensic Medicine › Genetic factors in colorectal cancer
- Health Sciences › Medicine › Oncology › Pancreatic and Hepatic Oncology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › BRCA gene mutations in cancer
- Keywords
- Lynch syndrome, pancreatic cancer, germline mutations, familial cancer risk, cumulative cancer risk, extracolonic tumors, cancer surveillance, segregation analysis
- MeSH terms
- MutL Protein Homolog 1, Adult, Aged, Aged, 80 and over, Colorectal Neoplasms, Hereditary Nonpolyposis, DNA Mutational Analysis, DNA-Binding Proteins, Female, Genotype, Humans, Male, Middle Aged, Nuclear Proteins, Pancreatic Neoplasms, Pedigree, Phenotype, Registries, Risk, Proportional Hazards Models, Germ-Line Mutation, SEER Program, Adaptor Proteins, Signal Transducing, MutS Homolog 2 Protein, DNA Mismatch Repair, Young Adult
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