{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,10]],"date-time":"2026-02-10T17:48:03Z","timestamp":1770745683953,"version":"3.49.0"},"reference-count":48,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2006,3,21]],"date-time":"2006-03-21T00:00:00Z","timestamp":1142899200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Molecular Carcinogenesis"],"published-print":{"date-parts":[[2006,5]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Cholangiocarcinoma (CCA) induced by liver fluke (<jats:italic>Opisthorchis viverrini<\/jats:italic>, Ov) infection is one of the most common and serious disease in northeast Thailand. To elucidate the molecular mechanism of cholangiocarcinogenesis induced by Ov infection, we employed a hamster model of CCA induced by Ov and <jats:italic>N<\/jats:italic>\u2010nitrosodimethylamine and analyzed candidate genes involved in CCA using fluorescence differential display\u2010PCR. Of 149 differentially amplified bands we identified, the upregulation of 23 transcripts and downregulation of 1 transcript related to CCA hamsters were confirmed by a reverse northern macroarray blot. The upregulated genes include signal transduction protein kinase A regulatory subunit I\u03b1 (<jats:italic>Prkar1a<\/jats:italic>), myristoylated alanine\u2010rich protein kinase C substrate, transcriptional factor LIM\u20104\u2010only domain, oxysterol\u2010binding protein involved in lipid metabolism, splicing regulatory protein 9, ubiquitin conjugating enzyme involved in protein degradation, \u03b2 tubulin, \u03b2 actin, and collagen type VI. Quantitative real\u2010time PCR confirmed that the expression of <jats:italic>Prkar1a<\/jats:italic> was significantly higher in CCA and its precursor lesion when compared with normal liver and normal gall bladder epithelia (<jats:italic>P<\/jats:italic>\u2009&lt;\u20090.05). <jats:italic>Prkar1a<\/jats:italic> expression tended to increase along with the progression of biliary transformation from hyperplasia and precancerous lesions to carcinoma. These findings contribute to our understanding of the processes involved in the molecular carcinogenesis of CCA in order to provide a unique perspective on the development of new chemotherapeutics in future. \u00a9 2006 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/mc.20094","type":"journal-article","created":{"date-parts":[[2006,3,21]],"date-time":"2006-03-21T07:32:39Z","timestamp":1142926359000},"page":"279-287","source":"Crossref","is-referenced-by-count":57,"title":["Altered gene expression in <i>Opisthorchis viverrini<\/i>\u2010associated cholangiocarcinoma in hamster 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