{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,13]],"date-time":"2026-07-13T16:03:42Z","timestamp":1783958622412,"version":"3.55.0"},"reference-count":48,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2014,7,16]],"date-time":"2014-07-16T00:00:00Z","timestamp":1405468800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J Hepato Biliary Pancreat"],"published-print":{"date-parts":[[2014,10]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>We investigated the aberrant expression of the <jats:styled-content style=\"fixed-case\">STAT<\/jats:styled-content> family in humans and liver fluke (<jats:italic><jats:styled-content style=\"fixed-case\">O<\/jats:styled-content>pisthorchis viverrini<\/jats:italic>, <jats:styled-content style=\"fixed-case\">O<\/jats:styled-content>v)\u2010induced hamster cholangiocarcinoma (<jats:styled-content style=\"fixed-case\">CCA<\/jats:styled-content>) tissues.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>The expression and phosphorylation of <jats:styled-content style=\"fixed-case\">STAT1<\/jats:styled-content>, <jats:styled-content style=\"fixed-case\">STAT2<\/jats:styled-content>, <jats:styled-content style=\"fixed-case\">STAT3<\/jats:styled-content>, <jats:styled-content style=\"fixed-case\">STAT4<\/jats:styled-content>, <jats:styled-content style=\"fixed-case\">STAT5a<\/jats:styled-content>, <jats:styled-content style=\"fixed-case\">STAT5b<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">STAT6<\/jats:styled-content> in human hamster <jats:styled-content style=\"fixed-case\">CCA<\/jats:styled-content> tissues were immunohistochemistry\u2010profiled. Localizations of <jats:styled-content style=\"fixed-case\">STAT5<\/jats:styled-content> in macrophages and lipopolysaccharide (<jats:styled-content style=\"fixed-case\">LPS)<\/jats:styled-content>\u2010induced macrophage\u2010conditioned media mediated <jats:styled-content style=\"fixed-case\">STAT3<\/jats:styled-content> activation in <jats:styled-content style=\"fixed-case\">CCA<\/jats:styled-content> cells were demonstrated.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>The expressions of <jats:styled-content style=\"fixed-case\">STAT<\/jats:styled-content> 1\u20134 and 6 were detected in the cytoplasm of hyperplastic bile ducts and tumor cells, whereas <jats:styled-content style=\"fixed-case\">STAT5a<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">STAT5b<\/jats:styled-content> were observed in macrophages and connective tissues surrounding tumor, respectively. The expressions of <jats:styled-content style=\"fixed-case\">STAT3<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">STAT5b<\/jats:styled-content> were significantly observed in tumors with a poorer histological differentiation. <jats:styled-content style=\"fixed-case\">STAT3<\/jats:styled-content> expression was significantly associated with shorter survival of <jats:styled-content style=\"fixed-case\">CCA<\/jats:styled-content> patients and was predominately activated in <jats:styled-content style=\"fixed-case\">CCA<\/jats:styled-content> cell lines. In the <jats:styled-content style=\"fixed-case\">CCA<\/jats:styled-content>\u2010hamsters, <jats:styled-content style=\"fixed-case\">STAT<\/jats:styled-content>s expression was gradually increased along the carcinogenesis, especially at 30 days post\u2010infection in which the inflammatory response was markedly observed, showing the correlation between the inflammation and <jats:styled-content style=\"fixed-case\">STAT<\/jats:styled-content>s activation. Moreover, <jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content>\u2010induced macrophage\u2010conditioned media could mediate <jats:styled-content style=\"fixed-case\">STAT3<\/jats:styled-content> activation in <jats:styled-content style=\"fixed-case\">CCA<\/jats:styled-content> cells.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p><jats:styled-content style=\"fixed-case\">STAT3<\/jats:styled-content> is the major <jats:styled-content style=\"fixed-case\">STAT,<\/jats:styled-content> which plays roles in the inflammation that contributes to <jats:styled-content style=\"fixed-case\">CCA<\/jats:styled-content> carcinogenesis and progression and may serve as a marker for a poor prognosis of <jats:styled-content style=\"fixed-case\">CCA<\/jats:styled-content>.<\/jats:p><\/jats:sec>","DOI":"10.1002\/jhbp.131","type":"journal-article","created":{"date-parts":[[2014,7,16]],"date-time":"2014-07-16T10:49:44Z","timestamp":1405507784000},"page":"767-776","source":"Crossref","is-referenced-by-count":40,"title":["<scp>STAT<\/scp>s profiling reveals predominantly\u2010activated <scp>STAT3<\/scp> in cholangiocarcinoma genesis and progression"],"prefix":"10.1002","volume":"21","author":[{"given":"Hasaya","family":"Dokduang","sequence":"first","affiliation":[{"name":"Department of Biochemistry Faculty of Medicine Khon Kaen University  Khon Kaen 40002 Thailand"},{"name":"Liver Fluke and Cholangiocarcinoma Research Center Khon Kaen University  Khon Kaen Thailand"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anchalee","family":"Techasen","sequence":"additional","affiliation":[{"name":"Center for Research Development of Medical Diagnostic Laboratories Faculty of Associated Medical Science 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