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Examination of ATM, BRCA1, and BRCA2 promoter methylation in patients with pancreatic cancer
- Source :
- Pancreatology
- Publication Year :
- 2021
- Publisher :
- Elsevier BV, 2021.
-
Abstract
- Background Pancreatic cancer is a lethal disease with a poor 5-year survival rate. Pathogenic germline variants in the coding regions of ATM, BRCA1, and BRCA2 are found in up to 4.8% of pancreatic cancer patients. Germline promoter methylation and gene silencing arising from a germline variant or through other mechanisms have been described as a cause of tumor suppressor gene inactivation. Methods We measured the level of promoter methylation of the ATM, BRCA1, and BRCA2 genes in peripheral blood lymphocytes from 655 patients with pancreatic cancer using real-time PCR. Results No evidence of germline promoter methylation of any of these genes was found. Promoter methylation levels were minimal with no patient having promoter methylation greater than 3.4%, 3.3%, and 7.6% for ATM, BRCA1 and BRCA2, respectively, well below levels found in patients who have inherited promoter methylation (∼50%). Conclusions We found no evidence of germline promoter methylation for the pancreatic susceptibility genes ATM, BRCA1 and BRCA2 in patients with pancreatic cancer. This study reveals that constitutive germline methylation of promoter CpG islands is rare in pancreatic cancer.
- Subjects :
- endocrine system diseases
Endocrinology, Diabetes and Metabolism
Genes, BRCA2
Breast Neoplasms
Ataxia Telangiectasia Mutated Proteins
Article
Germline
Pancreatic cancer
medicine
Humans
Gene silencing
Genetic Predisposition to Disease
Promoter Regions, Genetic
skin and connective tissue diseases
Gene
BRCA2 Protein
Hepatology
BRCA1 Protein
business.industry
Gastroenterology
Cancer
Methylation
DNA Methylation
medicine.disease
Pancreatic Neoplasms
medicine.anatomical_structure
CpG site
Cancer research
Female
Pancreas
business
Subjects
Details
- ISSN :
- 14243903
- Volume :
- 21
- Database :
- OpenAIRE
- Journal :
- Pancreatology
- Accession number :
- edsair.doi.dedup.....8f4887ec57b16801362bedf82457c07e