ArticleFrontiers in oncology2023
Role of pancreatic ductal adenocarcinoma risk factors in intraductal papillary mucinous neoplasm progression.
Article in Frontiers in oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 22 citations in OpenAlex.
- Pancreatic Cystic Neoplasm Risk Among Individuals With Diabetes.JAMA network open · 2026Article
- Preoperative malignancy risk assessment in pancreatic cystic neoplasms using clinical and laboratory parameters.World journal of gastrointestinal surgery · 2025Article
- DNA Damage and Repair in Pancreatic Cancer-The Latest Findings.International journal of molecular sciences · 2025Review
- Review
- Artificial intelligence in pancreatic intraductal papillary mucinous neoplasm imaging: A systematic review.PLOS digital health · 2025Article
- Article
- Translating the multifaceted use of liquid biopsy to management of early disease in pancreatic adenocarcinoma.Frontiers in oncology · 2025Review
- Genotypes of carboxypeptidase A1 and gamma-glutamyltransferase 1 may be useful tools for the diagnosis and the predictor of worrisome features of intraductal papillary mucinous neoplasm in Japan.JGH open : an open access journal of gastroenterology and hepatology · 2024Article
- Pancreatic Cancer: A Review of Risk Factors.Life (Basel, Switzerland) · 2024Review
- Dysbiosis Signature of Fecal Microbiota in Patients with Pancreatic Adenocarcinoma and Pancreatic Intraductal Papillary Mucinous Neoplasms.Biomedicines · 2024Article
- Molecular Pathology of Pancreatic Cystic Lesions with a Focus on Malignant Progression.Cancers · 2024Review
- A Simple Overview of Pancreatic Cancer Treatment for Clinical Oncologists.Current oncology (Toronto, Ont.) · 2023Review
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Authors and funding
15 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Pancreatic ductal adenocarcinoma (PDAC) is lethal due to its late diagnosis and lack of successful treatments. A possible strategy to reduce its death burden is prevention. Intraductal papillary mucinous neoplasms (IPMNs) are precursors of PDAC. It is difficult to estimate the incidence of IPMNs because they are asymptomatic. Two recent studies reported pancreatic cysts in 3% and 13% of scanned subjects. The possibility of identifying a subgroup of IPMN patients with a higher probability of progression into cancer could be instrumental in increasing the survival rate. In this study, genetic and non-genetic PDAC risk factors were tested in a group of IPMN patients under surveillance. Methods: A retrospective study was conducted on 354 IPMN patients enrolled in two Italian centres with an average follow-up of 64 months. With the use of DNA extracted from blood, collected at IPMN diagnosis, all patients were genotyped for 30 known PDAC risk loci. The polymorphisms were analysed individually and grouped in an unweighted polygenic score (PGS) in relation to IPMN progression. The ABO blood group and non-genetic PDAC risk factors were also analysed. IPMN progression was defined based on the development of worrisome features and/or high-risk stigmata during follow-up. Results: Two genetic variants (rs1517037 and rs10094872) showed suggestive associations with an increment of IPMN progression. After correction for multiple testing, using the Bonferroni correction, none of the variants showed a statistically significant association. However, associations were observed for the non-genetic variables, such as smoking status, comparing heavy smokers with light smokers (HR = 3.81, 95% 1.43-10.09, Conclusion: In conclusion, this study is the first attempt to investigate the presence of shared genetic background between PDAC risk and IPMN progression; however, the results suggest that the 30 established PDAC susceptibility polymorphisms are not associated with clinical IPMN progression in a sample of 354 patients. However, we observed indications of cigarette smoking and body mass index (BMI) involvement in IPMN progression. The biological mechanism that could link these two risk factors to progression could be chronic inflammation, of which both smoking and obesity are strong promoters.
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