A R G Sheel1, S Harrison1, I Sarantitis1, J A Nicholson1, T Hanna1, C Grocock1, M Raraty1, J Ramesh2, A Farooq3, E Costello1, R Jackson1, M Chapman4, A Smith5, R Carter6, C Mckay6, Z Hamady7, G P Aithal8, R Mountford9, P Ghaneh1, P Hammel10, M M Lerch11, C Halloran1, S P Pereira4, W Greenhalf1. 1. Department of Molecular and Clinical Cancer Medicine, Institute of Translational Medicine, University of Liverpool, Liverpool, L69 3GA, UK. 2. Department of Gastroenterology, The Royal Liverpool University Hospital, London, UK. 3. Department of Radiology, The Royal Liverpool University Hospital, London, UK. 4. Institute for Liver & Digestive Health, University College London, London, UK. 5. Department of Pancreatico-Biliary Surgery, Leeds Teaching Hospital Trust, Leeds, UK. 6. West of Scotland Pancreatic unit, Glasgow Royal Infirmary, Glasgow, UK. 7. Department of Hepatobiliary and Pancreatic Diseases, University Hospital Southampton, Southampton, UK. 8. NIHR Nottingham Biomedical Research Centre, Nottingham University Hospitals NHS Trust and University of Nottingham, Nottingham, NG7 2UH, UK. 9. Mersey Regional Molecular Genetics Laboratory, Liverpool Women's Hospital, Liverpool, UK. 10. Service de Gastroentérologie-Pancréatologie, Pôle des Maladies de l'Appareil Digestif, Hôpital Beaujon, 92118, Clichy Cedex, France. 11. Department of Medicine A, University Medicine Greifswald, Sauerbruch-Strasse, 17475, Greifswald, Germany.
Abstract
OBJECTIVES: Intraductal papillary mucinous neoplasms (IPMNs) are associated with risk of pancreatic ductal adenocarcinoma (PDAC). It is unclear if an IPMN in individuals at high risk of PDAC should be considered as a positive screening result or as an incidental finding. Stratified familial pancreatic cancer (FPC) populations were used to determine if IPMN risk is linked to familial risk of PDAC. METHODS: This is a cohort study of 321 individuals from 258 kindreds suspected of being FPC and undergoing secondary screening for PDAC through the European Registry of Hereditary Pancreatitis and Familial Pancreatic Cancer (EUROPAC). Computerised tomography, endoscopic ultrasound of the pancreas and magnetic resonance imaging were used. The risk of being a carrier of a dominant mutation predisposing to pancreatic cancer was stratified into three even categories (low, medium and high) based on: Mendelian probability, the number of PDAC cases and the number of people at risk in a kindred. RESULTS: There was a median (interquartile range (IQR)) follow-up of 2 (0-5) years and a median (IQR) number of investigations per participant of 4 (2-6). One PDAC, two low-grade neuroendocrine tumours and 41 cystic lesions were identified, including 23 IPMN (22 branch-duct (BD)). The PDAC case occurred in the top 10% of risk, and the BD-IPMN cases were evenly distributed amongst risk categories: low (6/107), medium (10/107) and high (6/107) (P = 0.63). CONCLUSIONS: The risk of finding BD-IPMN was independent of genetic predisposition and so they should be managed according to guidelines for incidental finding of IPMN.
OBJECTIVES: Intraductal papillary mucinous neoplasms (IPMNs) are associated with risk of pancreatic ductal adenocarcinoma (PDAC). It is unclear if an IPMN in individuals at high risk of PDAC should be considered as a positive screening result or as an incidental finding. Stratified familial pancreatic cancer (FPC) populations were used to determine if IPMN risk is linked to familial risk of PDAC. METHODS: This is a cohort study of 321 individuals from 258 kindreds suspected of being FPC and undergoing secondary screening for PDAC through the European Registry of Hereditary Pancreatitis and Familial Pancreatic Cancer (EUROPAC). Computerised tomography, endoscopic ultrasound of the pancreas and magnetic resonance imaging were used. The risk of being a carrier of a dominant mutation predisposing to pancreatic cancer was stratified into three even categories (low, medium and high) based on: Mendelian probability, the number of PDAC cases and the number of people at risk in a kindred. RESULTS: There was a median (interquartile range (IQR)) follow-up of 2 (0-5) years and a median (IQR) number of investigations per participant of 4 (2-6). One PDAC, two low-grade neuroendocrine tumours and 41 cystic lesions were identified, including 23 IPMN (22 branch-duct (BD)). The PDAC case occurred in the top 10% of risk, and the BD-IPMN cases were evenly distributed amongst risk categories: low (6/107), medium (10/107) and high (6/107) (P = 0.63). CONCLUSIONS: The risk of finding BD-IPMN was independent of genetic predisposition and so they should be managed according to guidelines for incidental finding of IPMN.
Authors: Stephen P Pereira; Lucy Oldfield; Alexander Ney; Phil A Hart; Margaret G Keane; Stephen J Pandol; Debiao Li; William Greenhalf; Christie Y Jeon; Eugene J Koay; Christopher V Almario; Christopher Halloran; Anne Marie Lennon; Eithne Costello Journal: Lancet Gastroenterol Hepatol Date: 2020-03-02
Authors: Kasper A Overbeek; Iris J M Levink; Brechtje D M Koopmann; Femme Harinck; Ingrid C A W Konings; Margreet G E M Ausems; Anja Wagner; Paul Fockens; Casper H van Eijck; Bas Groot Koerkamp; Olivier R C Busch; Marc G Besselink; Barbara A J Bastiaansen; Lydi M J W van Driel; Nicole S Erler; Frank P Vleggaar; Jan-Werner Poley; Djuna L Cahen; Jeanin E van Hooft; Marco J Bruno Journal: Gut Date: 2021-04-05 Impact factor: 31.793