ArticleEuropean journal of human genetics : EJHG2018
Risk of multiple pancreatic cancers in CDKN2A-p16-Leiden mutation carriers.
Article in European journal of human genetics : EJHG, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Hereditary Pancreatic Cancer: Genetic Risk, Surveillance Strategies, and Therapeutic Implications.International journal of molecular sciences · 2026Review
- Genetic risk factors in melanoma etiopathogenesis and the role of genetic counseling: A concise review.Bosnian journal of basic medical sciences · 2022Review
- Current status of inherited pancreatic cancer.Hereditary cancer in clinical practice · 2022Review
- The genetics of ductal adenocarcinoma of the pancreas in the year 2020: dramatic progress, but far to go.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2020Review
- Review
- Pathogenesis of multiple pancreatic cancers involves multicentric carcinogenesis and intrapancreatic metastasis.Cancer science · 2020Article
- Article
- Targeted next-generation sequencing reveals recurrence-associated genomic alterations in early-stage non-small cell lung cancer.Oncotarget · 2018Article
- Screening for pancreatic cancer has the potential to save lives, but is it practical?Expert review of gastroenterology & hepatologyReview
Corrections and comments
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CDKN2A-p16-Leiden mutation carriers have a substantial risk of developing pancreatic ductal adenocarcinoma (PDAC). One of the main clinical features of hereditary cancer is the development of multiple cancers. Since 2000, we have run a surveillance program for CDKN2A-p16-Leiden mutation carriers. The patients are offered a yearly MRI with optionally endoscopic ultrasound. In patients with a confirmed lesion, usually, a partial resection of the pancreas is recommended. A total of 18 PDAC (8.3%) were detected in 218 mutation carriers. In this report, we describe two CDKN2A-p16-Leiden patients with a synchronous and metachronous PDAC. Including two previously-reported cases, we identified four patients with multiple PDAC: two of 18 patients within the surveillance program (11%) and two patients with a proven CDKN2A-p16-Leiden mutation not participating in the surveillance program. In conclusion, this study demonstrated a high risk of developing multiple PDAC in CDKN2A-p16-Leiden mutation carriers. After detecting a primary tumor, it is very important to exclude the presence of a second synchronous tumor. Moreover, after a partial pancreatectomy for PDAC, close surveillance is necessary. In view of the current findings, offering a total pancreatectomy might be an appropriate option in patients with an early PDAC.
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