{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T09:09:18Z","timestamp":1791104958766,"version":"4.1.0"},"reference-count":33,"publisher":"American Association for Cancer Research (AACR)","issue":"16","content-domain":{"domain":["aacrjournals.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2004,8,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>We have established a primary pancreatic duct epithelial cell culture (PDEC) system to investigate the relationship between oncogenic activation of K-ras and pancreatic ductal tumorigenesis. We have found that the acute introduction of physiological levels of oncogenic K-ras (K-rasV12) into quiescent PDECs stimulates S-phase entry and induces a pronounced increase in cell size. Both effects are dependent on the functional integrity of the phosphatidylinositol 3\u2032-kinase (PI3K)\/mammalian target of rapamycin (mTOR) signaling pathway. In addition, K-rasV12 promotes the loss of epithelial E-cadherin and the gain of mesenchymal N-cadherin in PDEC. Our observations indicate that the oncogenic activation of K-ras is sufficient to elicit mitogenic and morphogenic responses in pancreatic ductal cells and hence is likely to play an instructive role in the initiation of pancreatic ductal adenocarcinoma.<\/jats:p>","DOI":"10.1158\/0008-5472.can-04-0807","type":"journal-article","created":{"date-parts":[[2005,9,20]],"date-time":"2005-09-20T22:41:36Z","timestamp":1127256096000},"page":"5659-5663","update-policy":"https:\/\/doi.org\/10.1158\/crossmark_policy","source":"Crossref","is-referenced-by-count":73,"title":["Oncogenic K-ras Drives Cell Cycle Progression and Phenotypic Conversion of Primary Pancreatic Duct Epithelial Cells"],"prefix":"10.1158","volume":"64","author":[{"given":"Cristina","family":"Agbunag","sequence":"first","affiliation":[{"name":"1Graduate Program in Molecular and Cellular Biology,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dafna","family":"Bar-Sagi","sequence":"additional","affiliation":[{"name":"1Graduate Program in Molecular and Cellular Biology,"},{"name":"2Department of Molecular Genetics and Microbiology, State University of New York at Stony Brook, Stony Brook, New York"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1086","published-online":{"date-parts":[[2004,8,16]]},"reference":[{"key":"2022061620214352000_B1","doi-asserted-by":"crossref","unstructured":"Jemal A, Murray T, Samuels A, Ghafoor A, Ward E, Thun MJ Cancer statistics, 2003. 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