Strong promoting effect of Opisthorchis viverrini infection on dimethylnitrosamine-initiated hamster liver

Thamavit, Witaya; Pairojkul, Chawalit; Tiwawech, Danai; Shirai, Tomoyuki; Ito, Nobuyuki

doi:10.1016/0304-3835(94)90040-x

Cited by 51 publications

(40 citation statements)

References 13 publications

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“…which combine tumor initiating doses of carcinogenic nitrosamines with Opisthorchis viverrini or Clonorchis sinensis infection [78][79][80][81][82] as a means to investigate the role of aberrant ErbB family receptor signaling in intrahepatic cholangiocarcinoma development and progression. This may be due to the fact that only very limited hamsterspecific immunochemical and molecular reagents are currently available for such studies.…”

Section: Sirica Ae Erbb Receptors and Cholangiocarcinoma 7041mentioning

confidence: 99%

Role of ErbB family receptor tyrosine kinases in intrahepatic cholangiocarcinoma

Sirica¹

2008

WJG

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Aberrant expression and signaling of epidermal growth factor receptor (ErbB) family receptor tyrosine kinases, most notably that of ErbB2 and ErbB1, have been implicated in the molecular pathogenesis of intrahepatic cholangiocarcinoma. Constitutive overexpression of ErbB2 and/or ErbB1 in malignant cholangiocytes has raised interest in the possibility that agents which selectively target these receptors could potentially be effective in cholangiocarcinoma therapy. However, current experience with such ErbBdirected therapies have at best produced only modest responses in patients with biliary tract cancers. This review provides a comprehensive and critical analysis of both preclinical and clinical studies aimed at assessing the role of altered ErbB2 and/or ErbB1 expression, genetic modifications, and dysregulated signaling on cholangiocarcinoma development and progression. Specific limitations in experimental approaches that have been used to assess human cholangiocarcinoma specimens for ErbB2 and/or ErbB1 overexpression and gene amplification are discussed. In addition, current rodent models of intrahepatic cholangiocarcinogenesis associated with constitutive ErbB2 overexpression are reviewed. Select interactive relationships between ErbB2 or ErbB1 with other relevant molecular signaling pathways associated with intrahepatic cholangiocarcinoma development and progression are also detailed, including those linking ErbB receptors to bile acid, cyclooxygenase-2, i n t e r l e u k i n -6 / g p 1 3 0 , t ra n s m e m b ra n e m u c i n s , hepatocyte growth factor/Met, and vascular endothelial growth factor signaling. Lastly, various factors that can limit therapeutic efficacy of ErbB-targeted agents against cholangiocarcinoma are considered.

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Section: Sirica Ae Erbb Receptors and Cholangiocarcinoma 7041mentioning

confidence: 99%

Role of ErbB family receptor tyrosine kinases in intrahepatic cholangiocarcinoma

Sirica¹

2008

WJG

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“…In addition, secretion or excretion of metabolic products from the liver fluke results in chronic irritation, hyperplasia and adenomatous changes of the bile duct epithelium [9] . Subsequent DNA damage in the biliary epithelium may drive malignant transformation [7,11] . To date, knowledge of the molecular basis of carcinogenesis and pathogenesis of CCA is limited.…”

Section: Introductionmentioning

confidence: 99%

Trefoil factors: Tumor progression markers and mitogens via EGFR/MAPK activation in cholangiocarcinoma

Kosriwong

Menheniott²,

Giraud³

et al. 2011

WJG

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AIM:To investigate trefoil factor (TFF ) gene copy number, mRNA and protein expression as potential biomarkers in cholangiocarcinoma (CCA). METHODS:TFF mRNA levels, gene copy number and protein expression were determined respectively by quantitative reverse transcription polymerase chain reaction (PCR), quantitative PCR and immunohistochemistry in bile duct epithelium biopsies collected from individuals with CCA, precancerous bile duct dysplasia and from disease-free controls. The functional impact of recombinant human (rh)TFF2 peptide treatment on proliferation and epidermal growth factor receptor (EGFR)/mitogenactivated protein kinase (MAPK) signaling was assessed in the CCA cell line, KMBC, by viable cell counting and immunoblotting, respectively. RESULTS: TFF1 , TFF2 and TFF3 mRNA expression was significantly increased in CCA tissue compared to disease-free controls, and was unrelated to gene copy number. TFF1 immunoreactivity was strongly increased in both dysplasia and CCA, whereas TFF2 immunoreactivity was increased only in CCA compared to diseasefree controls. By contrast, TFF3 immunoreactivity was moderately decreased in dysplasia and further decreased in CCA. Kaplan-Meier analysis found no association of TFF mRNA, protein and copy number with age, gender, histological subtype, and patient survival time. Treatment of KMBC cells with rhTFF2 stimulated proliferation, triggered phosphorylation of EGFR and downstream extracellular signal related kinase (ERK), whereas co-incubation with the EGFR tyrosine kinase inhibitor, PD153035, blocked rhTFF2-dependent proliferation and EGFR/ERK responses.CONCLUSION: TFF mRNA/protein expression is indicative of CCA tumor progression, but not predictive for histological sub-type or survival time. TFF2 is mitogenic in CCA via EGFR/MAPK activation.

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“…Furthermore, neither BOP (in females and males) nor DMN (in males) caused any neoplastic (or even non-neoplastic) liver cholangiocellular lesions with or without the subsequent ANIT administration. This may be due to the lack of initiating activity of BOP or DMN in rats, in contrast to hamsters [3][4][5][6][7][8] , and/or the lack of promoting activity of ANIT. At the dose employed here, 200 ppm, PCNA-positive bile duct epithelial cells did not increase in spite of bile duct proliferation.…”

Section: Discussionmentioning

confidence: 99%

“…It is therefore necessary to assess detailed mechanisms in appropriate animal models to establish mechanism-based strategies to control human ICC. A number of animal models of ICC have been developed in hamsters using combinations of chemical carcinogens, Opisthorchis infection and bile duct ligation [3][4][5][6][7][8] . However, only limited information is available about the genetic background of hamsters.…”

Section: Introductionmentioning

confidence: 99%

“…In this context, the present study was performed to investigate the effects of ANIT on the liver with or without initiating treatment with N-nitrosobis(2-oxopropyl)amine (BOP) or Nnitrosodimethylamine (DMN). BOP and DMN were selected, because both of them have been used in hamster ICC models [3][4][5][6][7][8] . Male hamsters have been used in previous experiments to produce ICC 4,7 , so we used only male animals in investigations using DMN.…”

Section: Introductionmentioning

confidence: 99%

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.ALPHA.-Naphthylisothiocyanate Induces Intrahepatic Bile Duct with Greater Proliferation in Female Rats than in Males

et al. 2004

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Abstract:The present study was conducted with the original purpose of investigating the possibility that α-naphthylisothiocyanate (ANIT) might induce intrahepatic cholangiocellular neoplasms in rats after appropriate carcinogenesis-initiating treatments, based on its known effect of causing intrahepatic bile duct proliferation. Fischer 344 rats (6 weeks old) were given 3 weekly intraperitoneal administrations of vehicle (female and male), N-nitrosobis(2-oxopropyl)amine (BOP) (20 mg/kg body weight, female and male) or N-nitrosodimethylamine (DMN) (10 mg/kg body weight, male only), and fed a basal diet with or without 200 ppm of ANIT from the commencement for up to 24 weeks. Animals were sequentially sacrificed at the ends of weeks 8, 16 and 24 to examine morphological changes in the liver. ANIT caused proliferation of intrahepatic bile duct epithelial cells with no atypia when administered alone or in combination with BOP (female and male) or DMN (male only), while neither BOP nor DMN caused bile duct proliferation per se or altered the magnitude of the effect of ANIT. The degree of bile duct proliferation caused by ANIT was greater in females than in males. No hepatocellular or liver (pre)neoplastic changes were observed. These results indicate that although ANIT does not induce any neoplastic changes in the liver even after initiation with BOP (female and male) or DMN (male), it causes non-neoplastic intrahepatic bile duct proliferation with a clear sex difference. (J Toxicol Pathol 2004; 17: 205-210)

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Strong promoting effect of Opisthorchis viverrini infection on dimethylnitrosamine-initiated hamster liver

Cited by 51 publications

References 13 publications

Role of ErbB family receptor tyrosine kinases in intrahepatic cholangiocarcinoma

Role of ErbB family receptor tyrosine kinases in intrahepatic cholangiocarcinoma

Trefoil factors: Tumor progression markers and mitogens via EGFR/MAPK activation in cholangiocarcinoma

.ALPHA.-Naphthylisothiocyanate Induces Intrahepatic Bile Duct with Greater Proliferation in Female Rats than in Males

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