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However, whether <jats:italic>H<\/jats:italic>. <jats:italic>pylori<\/jats:italic> infection promotes CCA development remains unknown. We investigated CCA development in hamsters induced by a combination of infection with <jats:italic>H<\/jats:italic>. <jats:italic>pylori<\/jats:italic> and administration of <jats:italic>N<\/jats:italic>\u2010nitrosodimethylamine (NDMA) and compared findings with those in an OV plus NDMA group.<\/jats:p><\/jats:sec><jats:sec><jats:title>Materials and Methods<\/jats:title><jats:p>Eighty\u2010five hamsters were divided into four groups: (1) normal, (2) administered NDMA, (3) infected with <jats:italic>cagA<\/jats:italic><jats:sup>+<\/jats:sup> <jats:italic>H<\/jats:italic>. <jats:italic>pylori<\/jats:italic> and administered NDMA (HN group), and (4) infected with OV and administered NDMA (ON group). Animals were euthanized at 3 and 6\u00a0months post\u2010infection. Histopathological changes of liver and the expression of markers associated with carcinogenesis were studied.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>At 3\u00a0months post\u2010infection (p.i.), cholangitis and lymphoid follicles without tumor appearance were noted in the HN group, whereas extensive fibrosis was seen in members of the ON group, 10% of which had developed tumors. At 6\u00a0months p.i., 10% of hamsters administered NDMA alone had developed CCA, whereas in the HN and ON groups, 20% and 60% of hamsters, respectively, had developed CCA. Cytokeratin\u201019 (CK19) expression was observed in the CCA tissues of both the HN and the ON groups, confirming the bile duct origin of the CCA cells. CCA development in the HN group might be inflammation\u2010mediated, as suggested by overexpression of HMGB1, PCNA, <jats:italic>IL<\/jats:italic>\u2010<jats:italic>8<\/jats:italic>, and 8\u2010OxodG in CCA tissues.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p><jats:italic>cagA<\/jats:italic><jats:sup>+<\/jats:sup> <jats:italic>H<\/jats:italic>. <jats:italic>pylori<\/jats:italic> infection and carcinogen intake can induce CCA development with slow progression.<\/jats:p><\/jats:sec>","DOI":"10.1111\/hel.12817","type":"journal-article","created":{"date-parts":[[2021,5,25]],"date-time":"2021-05-25T04:56:13Z","timestamp":1621918573000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":13,"title":["CagA<sup>+<\/sup><i>Helicobacter pylori<\/i> infection and <i>N<\/i>\u2010nitrosodimethylamine administration induce cholangiocarcinoma development in 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