{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,27]],"date-time":"2026-10-27T20:45:45Z","timestamp":1793133945906,"version":"4.5.0"},"reference-count":35,"publisher":"American Medical Association (AMA)","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JAMA Surg"],"published-print":{"date-parts":[[2026,2,1]]},"abstract":"\n Importance<\/jats:title>\n Studying the molecular profiles of mixed-type and branch-duct (BD) intraductal papillary mucinous neoplasms (IPMNs) is important to understand the underlying biological basis for higher malignant potential of mixed-type IPMNs.<\/jats:p>\n <\/jats:sec>\n \n Objective<\/jats:title>\n To compare mutation patterns in mixed-type vs BD-IPMNs through cyst fluid next-generation sequencing (NGS) analysis using PancreaSeq NGS.<\/jats:p>\n <\/jats:sec>\n \n Design, Setting, and Participants<\/jats:title>\n \n For this cohort study, pancreatic cyst fluid specimens from 31 medical centers were sent to a centralized NGS lab for analysis between January 2018 and February 2020. Patients with IPMNs (based on\n KRAS<\/jats:italic>\n and\n GNAS<\/jats:italic>\n mutant status) and with available main pancreatic duct (MPD) size data were included. Patients with main-duct IPMNs and with MPD 10 mm or greater were excluded. Mixed-type IPMNs were defined as IPMNs with an MPD of 5 to 9 mm, and BD-IPMNs were defined as IPMNs with an MPD less than 5 mm. High-risk mutations (HRMs) were categorized as alterations in\n TP53<\/jats:italic>\n ,\n SMAD4<\/jats:italic>\n ,\n CTNNB1<\/jats:italic>\n , and\n mTOR<\/jats:italic>\n genes. Advanced neoplasia was defined as IPMNs with invasive carcinoma or high-grade dysplasia. Data were analyzed from June 1 to 5, 2025.\n <\/jats:p>\n <\/jats:sec>\n \n Main Outcomes and Measures<\/jats:title>\n Primary outcomes included rates of HRMs and the co-occurrence of 2 or more HRMs in mixed-type IPMNs and BD-IPMNs.<\/jats:p>\n <\/jats:sec>\n \n Results<\/jats:title>\n \n Among 674 patients with IPMNs, 202 had mixed-type IPMN, and 472 had BD-IPMN. There were 379 female patients (56.2%) and 295 male patients (43.8%); the mean (SD) age was 70.3 (9.6) years. HRMs were observed in 106 patients (16%), with\n TP53<\/jats:italic>\n ,\n SMAD4<\/jats:italic>\n , and\n MTOR<\/jats:italic>\n mutations more common in mixed-type IPMNs. Of the 674 patients, 167 patients underwent surgical resection, and these 167 patients had final surgical pathology available. Overall, mixed-type IPMNs had significantly higher rates of HRMs (62 [31%] vs 44 [9.3%];\n P<\/jats:italic>\n \u2009&amp;lt;\u2009.001) and co-occurrence of 2 or more HRMs (25 [12.4%] vs 14 [3%];\n P<\/jats:italic>\n \u2009&amp;lt;\u2009.001) compared with BD-IPMNs. On multivariate logistic regression, mixed-type IPMNs were independently associated with HRMs (odds ratio, 3.42; 95% CI, 1.72-6.82). Preoperative NGS detection of HRMs showed 90% sensitivity, 100% specificity, a positive predictive value (PPV) of 100%, and a negative predictive value (NPV) of 86% for predicting advanced neoplasia in mixed-type IPMNs. The presence of any worrisome feature or high-risk stigmata showed a sensitivity of 100%, very low specificity of 13.3%, PPV of 67%, and NPV of 100%.\n <\/jats:p>\n <\/jats:sec>\n \n Conclusions and Relevance<\/jats:title>\n This study found that mixed-type IPMNs are more likely to harbor HRMs associated with advanced neoplasia. Cyst fluid NGS is highly sensitive and specific for predicting advanced neoplasia in patients with mixed-type IPMNs and should therefore be considered to help upgrade or downgrade risk based on the presence or absence of other worrisome features.<\/jats:p>\n <\/jats:sec>","DOI":"10.1001\/jamasurg.2025.5692","type":"journal-article","created":{"date-parts":[[2025,12,23]],"date-time":"2025-12-23T16:00:31Z","timestamp":1766505631000},"page":"171","source":"Crossref","is-referenced-by-count":5,"title":["Molecular Analysis of Mixed-Type and Branch-Duct Intraductal Papillary Mucinous Neoplasms"],"prefix":"10.1001","volume":"161","author":[{"given":"Amudhan","family":"Kannan","sequence":"first","affiliation":[{"name":"Pancreatic Cancer Prevention Program, University of Texas Southwestern Medical Center, Dallas"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gilbert Z.","family":"Murimwa","sequence":"additional","affiliation":[{"name":"Pancreatic Cancer Prevention Program, 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Pennsylvania"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marina N.","family":"Nikiforova","sequence":"additional","affiliation":[{"name":"Department of Pathology, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alessandro","family":"Paniccia","sequence":"additional","affiliation":[{"name":"Department of Surgery, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Amer H.","family":"Zureikat","sequence":"additional","affiliation":[{"name":"Department of Surgery, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kenneth K.W.","family":"Lee","sequence":"additional","affiliation":[{"name":"Department of Surgery, University of Pittsburgh Medical Center, Pittsburgh, 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