Results of surveillance for hereditary pancreatic cancer using annual MRI (CP)

Wouter H. de Vos1, Martin N. Wasser2, Bert A. Bonsing3, Anneke M. van Mil4, Daniel W. Hommes1, Hans Morreau5, Hans F. Vasen1,6
Departments of Gastroenterology and Hepatology1, Radiology2, Surgery3, Clinical Genetics4, Pathology5 Leiden University Medical Center; Netherlands Foundation for the Detection of Hereditary Tumours, Leiden6

Surveillance for pancreatic cancer (PC) in high risk groups may lead to early detection and may improve overall survival. We screened for early pancreatic neoplasia in individuals with a p16- germline mutation or with a strong family history of PC (FPC).

Methods: High risk individuals were offered annual surveillance by Magnetic Resonance Imaging (MRI(CP)). In case of suspected lesions surgery or additional follow up (FU) was provided. In case of doubt, the examination was repeated within 2-4 months.

Results: 66 (28 male) individuals with an average age of 56 yrs (range 40-72) were studied (60 from p16-and 6 from FPC families). The median FU was 3.5 yrs (range 0-7). Four patients were diagnosed with PC (3 confirmed by histology). One patient was diagnosed with PC at base-line examination. She had a 1cm tail PC that was missed but clearly seen in retrospect. She developed liver metastases within 3 months. One patient had a corpus carcinoma on her second MRI (CP). Her previous MRI (CP) was of poor quality due to movement artefacts but 2 (possible) side branch IPMTs were present. She was found to have peritoneal metastases of a colonic carcinoid at surgery (in addition to PC). Another patient was diagnosed with a 1.5cm mass in the tail on his third screening. He underwent distal pancreatectomy. Histological examination showed PC with positive resection margins and 4 positive nodes. The fourth patient developed local dilatation of the pancreatic duct in the corpus on his third screening. Five months later, a 1cm mass was found. However, at the same time disseminated melanoma was diagnosed which was reason for not offering pancreatic surgery. One patient (FPC) underwent a Whipple resection for an intraductal papillary mucinous neoplasm (IPMN). (Possible-) IPMTs were present in at least five p16 carriers (8%) and in 3 patients from FPC families (50%). In 9 patients aspecific lesions were detected in the pancreas with MRI (CP). These could be classified as artefacts by repeated examination.

Conclusion: As in FPC patients, IPMTs are important precursor lesions to pancreatic cancer in p16 gene carriers. These small premalignant lesions can be identified by MRI(CP).

In view of the substantial morbidity and mortality of pancreatic surgery, a major challenge is to decide at what stage and to what extent a patient should undergo prophylactic surgery. Close observation of patients with pancreatic lesions could add valuable information to this question.