{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,11,2]],"date-time":"2025-11-02T16:23:45Z","timestamp":1762100625114},"reference-count":46,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2006,7,20]],"date-time":"2006-07-20T00:00:00Z","timestamp":1153353600000},"content-version":"vor","delay-in-days":4006,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Molecular Carcinogenesis"],"published-print":{"date-parts":[[1995,8]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>An investigation of <jats:italic>p53<\/jats:italic> gene mutation by single\u2010stranded conformation polymorphism analysis of polymerase chain reaction products followed by direct sequencing and of murine double minute 2 (<jats:italic>mdm\u20102<\/jats:italic>) gene amplification by Southern blot analysis was performed, using a series of hamster pancreatic duct adenocarcinomas: 18 primary adenocarcinomas induced by <jats:italic>N<\/jats:italic>\u2010nitrosobis(2\u2010oxopropyl)amine, a transplantable adenocarcinoma (HPD), and three cell lines derived from HPD (HPD1NR, HPD2NR, and HPD3NR). A mutation in the <jats:italic>p53<\/jats:italic> gene was detected at codon 197, resulting in an amino acid change from leucine to phenylalanine, in both HPD and the three cell lines but in none of the 18 primary adenocarcinomas. In the three HPD cell lines, which were confirmed to contain only cancer cells, a normal p53 gene allele was retained. Immunohistochemical investigation of p53 expression using polyclonal antibody Ab\u20107 revealed positive nuclear staining in the HPD and two back\u2010transplanted tumors derived from HPD1NR and HPD2NR but not in the 18 primary adenocarcinomas. <jats:italic>mdm\u20102<\/jats:italic> gene amplification was not detected in 18 primary adenocarcinomas or any of the tumor cell lines. The results suggest that a <jats:italic>p53<\/jats:italic> gene mutation without allelic loss, together with overexpression of p53 protein, may be a genetic alteration involved in the progression stage of multistep pancreatic carcinogenesis in hamsters and that <jats:italic>mdm\u20102<\/jats:italic> gene amplification is not important for this process. \u00a9 1995 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/mc.2940130409","type":"journal-article","created":{"date-parts":[[2007,2,21]],"date-time":"2007-02-21T20:56:59Z","timestamp":1172091419000},"page":"266-271","source":"Crossref","is-referenced-by-count":17,"title":["<i>p53<\/i> mutation without allelic loss and absence of <i>mdm<\/i>\u20102 amplification in a transplantable hamster pancreatic ductal adenocarcinoma and derived cell lines but not primary ductal adenocarcinomas in hamsters"],"prefix":"10.1002","volume":"13","author":[{"given":"Shunji","family":"Okita","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Masahiro","family":"Tsutsumi","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Morikazu","family":"Onji","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yoichi","family":"Konishi","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2006,7,20]]},"reference":[{"key":"e_1_2_1_2_2","doi-asserted-by":"publisher","DOI":"10.1038\/342705a0"},{"key":"e_1_2_1_3_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.1905840"},{"key":"e_1_2_1_4_2","doi-asserted-by":"publisher","DOI":"10.1038\/351453a0"},{"key":"e_1_2_1_5_2","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(89)90045-7"},{"key":"e_1_2_1_6_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.2144057"},{"key":"e_1_2_1_7_2","doi-asserted-by":"publisher","DOI":"10.1016\/0304-3835(93)90168-9"},{"key":"e_1_2_1_8_2","first-page":"1503","article-title":"Human 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