2012 ©
             Publication
Journal Publication
Title of Article CagA+ Helicobacter pylori infection and N-nitrosodimethylamine administration induce cholangiocarcinoma development in hamsters 
Date of Acceptance 5 May 2021 
Journal
     Title of Journal Helicobacter 
     Standard SCOPUS 
     Institute of Journal John Wiley & Sons Ltd 
     ISBN/ISSN DOI: 10.1111/hel.12817 
     Volume 2021 
     Issue Vol 27 
     Month
     Year of Publication 2021 
     Page  
     Abstract Background: Helicobacter pylori (HP) has been detected in the hepatobiliary tract of cholangiocarcinoma (CCA) patients in regions both endemic and non-endemic for Opisthorchis viverrini (OV) infection. However, whether H. pylori infection promotes CCA development remains unknown. We investigated CCA development in hamsters induced by a combination of infection with H. pylori and administration of N-nitrosodimethylamine (NDMA) and compared findings with those in an OV plus NDMA group. Materials and Methods: Eighty-five hamsters were divided into four groups: (1) normal, (2) administered NDMA, (3) infected with cagA+ H. pylori and administered NDMA (HN group), and (4) infected with OV and administered NDMA (ON group). Animals were euthanized at 3 and 6 months post-infection. Histopathological changes of liver and the expression of markers associated with carcinogenesis were studied. Results: At 3 months post-infection (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 months 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-19 ( CK-19) 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-mediated, as suggested by overexpression of HMGB1, PCNA, IL-8, and 8-OxodG in CCA tissues. Conclusion: cagA+ H. pylori infection and carcinogen intake can induce CCA development with slow progression.  
     Keyword Cholangiocarcinoma, Helicobacter pylori, Opisthorchis viverrini, histopathological study, risk factor, the animal model 
Author
607100003-1 Miss RUNGTIWA DANGTAKOT [Main Author]
Graduate School Doctoral Degree

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