LAUSR

Copyright distinct clinical entity and differ substantially from pancreatic ductal adenocarcinoma in terms of histology, genetic mutations, clinical features, and prognosis. They usually have a benign behavior, but some tumors have the potential for local invasion andmetastases. Unfortunately, there are no clear factors to predict poor outcomes, sowe conducted this retrospective analysis to further characterize and prognosticate malignant behavior and disease outcomes in patients with SPN. Patients 18 years and older with the histological diagnosis of SPN of the pancreas registered in the institutional tumor registry from 1992 to 2016 were selected for review. Demographic, clinical, imaging, and treatment datawere recorded. Pathology specimens were used to determine the variant of malignancy according to the World Health Organization 2010 criteria. Patients with nonmalignant and malignant tumors were compared in terms of the variables collected, which were analyzed looking for statistical significance, using Fisher, Wilcoxon, orχ test depending on the type of variable. Forty-two patients (95.4%) underwent surgical resection of SPN of the pancreas (28 nonmalignant and 14 malignant). Median age at diagnosis was 28 years (range, 13–64 years), and most were female (88.9%). Approximately one-third of the patients (31.8%) were asymptomatic at diagnosis. Themost frequent symptoms at presentation included abdominal pain (45.5%), followed by nausea or vomiting (9.1%) and back pain (6.8%). In patients whom carbohydrate antigen 19-9wasmeasured at the time of diagnosis, it waswithin normal range. Most tumors (59%) were located in the tail of the pancreas, with 27% and 18% of tumors located in the head and body, respectively. Median tumor sizewas 4.6 cm (range, 1.5–13.5 cm). Malignant tumors were more likely to have positive margins after resection (P = 0.031). There were no patients with macroscopic residual disease. None of these patients received adjuvant therapy. Among 24 patients who were tested, all of them were found to have CTNNB1 (β-catenin) mutations. Nextgeneration sequencing was performed in 2 patients. In addition to CTNNB1 mutations,MAGI2 and ATMmutations were observed in one patient and p53mutation was recorded in another patient. Themedian follow-upwas 115months (95% confidence interval, 69–172 months). Two patients (4.5%) developed recurrences after surgery (4.5%). Both patients had previous malignant tumor classifications, and they underwent additional surgeries for recurrences. One of the patients was without evidence of disease at last follow-up, and the other was alive with residual disease. Two patients (4.5%) initially presented with