{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,11,13]],"date-time":"2025-11-13T12:29:33Z","timestamp":1763036973261},"reference-count":34,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2016,5,2]],"date-time":"2016-05-02T00:00:00Z","timestamp":1462147200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"Ministry of Education, Science and Culture of Japan","award":["25462115"],"award-info":[{"award-number":["25462115"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Surgical Oncology"],"published-print":{"date-parts":[[2016,7]]},"abstract":"<jats:sec><jats:title>Background<\/jats:title><jats:p>Although various features of ampullary adenocarcinoma have been reported, the impact of genetic alterations and rare subtypes on clinical outcome remains unclear.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>We determined the expression of proteins, including MUC1, MUC2, p53, p16, Smad\/Dpc4, and \u03b2\u2010catenin, and genetic mutations such as <jats:italic>KRAS<\/jats:italic>, <jats:italic>BRAF<\/jats:italic>, and <jats:italic>GNAS<\/jats:italic> mutations in 69 patients with ampullary adenocarcinoma to clarify their relationships with clinicopathological findings and subtypes.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Kaplan\u2013Meier survival analysis indicated that abnormal p53 labeling was significantly associated with a shorter overall survival. MUC1<jats:italic>\u2010<\/jats:italic>positive and MUC2<jats:italic>\u2010<\/jats:italic>negative expressions were significantly associated with lymphatic invasion, pancreatic invasion, lymph node metastasis, and advanced UICC stage. The <jats:italic>KRAS<\/jats:italic> mutation was significantly associated with large tumor size and pancreatic invasion. There were 35 intestinal (50%), 15 pancreatobiliary (22%), and 11 mixed subtype (16%) tumors. Patients with the mixed subtype showed significantly poor outcome. The invasiveness of the mixed subtype was similar to that of the pancreatobiliary subtype; moreover, the mixed subtype showed a high incidence of abnormal \u03b2\u2010catenin immunolabeling (73%).<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Protein expression and genetic mutation are clinically associated with the characteristics of ampullary adenocarcinoma. The mixed subtype may have a distinct tumor nature as compared to other two major subtypes. <jats:italic>J. Surg. 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