{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,3]],"date-time":"2026-11-03T14:21:08Z","timestamp":1793715668675,"version":"4.6.1"},"reference-count":123,"publisher":"American Society for Clinical Investigation","issue":"14","license":[{"start":{"date-parts":[[2025,7,15]],"date-time":"2025-07-15T00:00:00Z","timestamp":1752537600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2025,7,15]]},"abstract":"<jats:p>Pancreatic ductal adenocarcinoma (PDAC) is known to progress from one of two main precursor lesions: pancreatic intraepithelial neoplasia (PanIN) or intraductal papillary mucinous neoplasm (IPMN). The poor survival rates for patients with PDAC, even those diagnosed with localized disease, highlight the need for pancreatic cancer interception at the precursor stage. Although their basic biological drivers are well characterized, practical strategies for PanIN and IPMN interception remain elusive due to difficulties with detection, risk stratification, and low-morbidity intervention. Recently, advances in liquid biopsy, spatial multiomics analysis, and machine learning technology have provided deeper understanding of the molecular landscapes underlying pancreatic precursor development and progression. In this Review, we outline the different histologic phenotypes, clinical characteristics, and neoplastic cell\u2013intrinsic and \u2013extrinsic drivers of PanINs and IPMNs, with particular focus on current and potential future opportunities for pancreatic precancer interception.<\/jats:p>","DOI":"10.1172\/jci191937","type":"journal-article","created":{"date-parts":[[2025,7,14]],"date-time":"2025-07-14T18:00:41Z","timestamp":1752516041000},"source":"Crossref","is-referenced-by-count":32,"title":["Early neoplastic lesions of the pancreas: initiation, progression, and opportunities for precancer interception"],"prefix":"10.1172","volume":"135","author":[{"given":"Brian A.","family":"Pedro","sequence":"first","affiliation":[{"name":"Department of Pathology, and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Laura D.","family":"Wood","sequence":"additional","affiliation":[{"name":"Department of Pathology, and"},{"name":"Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"232","published-online":{"date-parts":[[2025,7,15]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1097\/MPA.0000000000000701"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1001\/jamanetworkopen.2021.4708"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1158\/2159-8290.CD-24-0015"},{"key":"B4","unstructured":"American Cancer Society. 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