Source:http://linkedlifedata.com/resource/pubmed/id/17573895
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
8
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pubmed:dateCreated |
2007-6-27
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pubmed:abstractText |
In mice, 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) induces a high incidence of malignant lymphoma and leukemia, but exhibits little, if any, carcinogenic activity in the large intestine after long-term exposure. However, recent studies have revealed that colonic adenocarcinomas can be efficiently and rapidly induced by combined treatment with PhIP and dextran sulfate sodium (DSS), a potent inducer of colitis. In the present study, the authors investigated the effects of inflammation on PhIP-induced carcinogenesis using two mouse strains, C57BL/6J and MSM/Ms, showing distinct temporal profiles of inflammatory responses to DSS. A long-term carcinogenesis experiment conducted with a single i.g. administration of PhIP (200 mg/kg body weight), followed by DSS treatment in drinking water for 4-6 days, revealed an increase in tumor incidence in C57BL/6J mice in accordance with the DSS intake. In contrast, neoplastic lesions were rarely observed in the MSM/Ms strain. From the short-term exposure to DSS for 4 days, C57BL/6J mice demonstrated severe chronic colitis, accompanied by hyperplastic cryptal epithelium and extensive cellular infiltration. Splenomegaly and swelling of mesenteric lymph nodes were also evident for over 1 month as chronic symptoms of systemic immunological disturbance. However, no inflammatory lesions were detected in MSM/Ms mice. The present results provide strong evidence that prolonged chronic inflammatory responses induced by DSS are directly responsible for the observed enhancement of PhIP-induced large bowel carcinogenicity.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
1347-9032
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
98
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1157-63
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pubmed:meshHeading |
pubmed-meshheading:17573895-Adenocarcinoma,
pubmed-meshheading:17573895-Animals,
pubmed-meshheading:17573895-Carcinogenicity Tests,
pubmed-meshheading:17573895-Carcinogens,
pubmed-meshheading:17573895-Cocarcinogenesis,
pubmed-meshheading:17573895-Colitis,
pubmed-meshheading:17573895-Colon,
pubmed-meshheading:17573895-Colonic Neoplasms,
pubmed-meshheading:17573895-Dextran Sulfate,
pubmed-meshheading:17573895-Disease Susceptibility,
pubmed-meshheading:17573895-Imidazoles,
pubmed-meshheading:17573895-Intestinal Mucosa,
pubmed-meshheading:17573895-Mice,
pubmed-meshheading:17573895-Mice, Inbred BALB C,
pubmed-meshheading:17573895-Mice, Inbred Strains,
pubmed-meshheading:17573895-Species Specificity,
pubmed-meshheading:17573895-Time Factors
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pubmed:year |
2007
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pubmed:articleTitle |
Mouse strain differences in inflammatory responses of colonic mucosa induced by dextran sulfate sodium cause differential susceptibility to PhIP-induced large bowel carcinogenesis.
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pubmed:affiliation |
Biochemistry Division, National Cancer Center Research Institute, 5-1-1 Tsukiji, Tokyo 104-0045, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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