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Zinc deprivation promotes progression of 1,2-dimethylhydrazine-induced colon tumors but reduces malignant invasion in mice

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dc.contributor Wichita State University. Department of Public Health Sciences en_US
dc.contributor.author Carter, John W. en_US
dc.contributor.author Lancaster, Hugh K. en_US
dc.contributor.author Hardman, W. Elaine en_US
dc.contributor.author Cameron, Ivan L. en_US
dc.date.accessioned 2012-03-07T17:40:09Z
dc.date.available 2012-03-07T17:40:09Z
dc.date.issued 1997 en_US
dc.identifier 9101549 en_US
dc.identifier 7905040 en_US
dc.identifier T32 AG-00165 en_US
dc.identifier.citation Nutrition and cancer. 1997; 27(3): 217-21. en_US
dc.identifier.issn 0163-5581 en_US
dc.identifier.uri http://dx.doi.org/10.1080/01635589709514529 en_US
dc.identifier.uri http://hdl.handle.net/10057/4754
dc.description Click on the DOI link below to access the article (may not be free). en_US
dc.description.abstract The aim of this study was to characterize colon tumor development and invasiveness associated with dietary zinc deprivation. Colon carcinogenesis was initiated by eight weekly subcutaneous injections of 1,2-dimethylhydrazine (DMH) at 12 mg DMH base/kg body wt in groups of mice maintained on diets containing 30 micrograms/kg dietary zinc (zinc adequate, ZA) or 3 micrograms/kg dietary zinc (zinc deprived, ZD). All mice were killed 24 weeks after the last injection of DMH. Mean zinc concentration in the liver was significantly lower in the ZD group than in the ZA group. The total number of grossly detectable colon tumors was the same in both dietary groups. However, histopathological study of each tumor revealed significantly more adenomatous polyps (AP) and invasive adenocarcinomas (CA) in the ZA group, whereas the ZD group had significantly more noninvasive carcinomas in situ (CIS). It appears that zinc deprivation stimulated progression of AP to noninvasive CIS but retarded the progression of noninvasive CIS to invasive CA. Immunohistochemistry of tumors from ZA and ZD mice indicated increased amounts of type IV collagenase in epithelial tumor cells and in stromal cells adjacent to tumor tissue regardless of the amount of dietary zinc consumed. It is suggested that zinc deprivation may limit function of zinc-requiring enzymes such as superoxide dismutase and type IV collagenase, resulting in enhanced progression of AP to noninvasive CIS and retardation of invasion of CIS to become CA, respectively. en_US
dc.description.sponsorship NIA NIH HHS en_US
dc.format.extent 217-21 en_US
dc.language.iso eng en_US
dc.publisher Routledge en_US
dc.relation.ispartofseries Nutrition and Cancer en_US
dc.relation.ispartofseries Nutr Cancer en_US
dc.source NLM en_US
dc.subject Research Support, Non-U.S. Gov't en_US
dc.subject Research Support, U.S. Gov't, Non-P.H.S. en_US
dc.subject Research Support, U.S. Gov't, P.H.S. en_US
dc.subject.mesh 1,2-Dimethylhydrazine en_US
dc.subject.mesh Adenocarcinoma/chemically induced en_US
dc.subject.mesh Animals en_US
dc.subject.mesh Body Weight en_US
dc.subject.mesh Carcinogens en_US
dc.subject.mesh Carcinoma in Situ/chemically induced en_US
dc.subject.mesh Collagenases/analysis en_US
dc.subject.mesh Colon/pathology en_US
dc.subject.mesh Colonic Neoplasms/chemically induced en_US
dc.subject.mesh Diet en_US
dc.subject.mesh Dimethylhydrazines en_US
dc.subject.mesh Immunohistochemistry en_US
dc.subject.mesh Liver/chemistry en_US
dc.subject.mesh Male en_US
dc.subject.mesh Matrix Metalloproteinase 9 en_US
dc.subject.mesh Mice en_US
dc.subject.mesh Neoplasm Invasiveness en_US
dc.subject.mesh Organ Size en_US
dc.subject.mesh Zinc/administration & dosage en_US
dc.subject.mesh Adenocarcinoma/pathology en_US
dc.subject.mesh Carcinoma in Situ/pathology en_US
dc.subject.mesh Collagenases/metabolism en_US
dc.subject.mesh Colonic Neoplasms/pathology en_US
dc.subject.mesh Zinc/analysis en_US
dc.subject.mesh Zinc/deficiency en_US
dc.title Zinc deprivation promotes progression of 1,2-dimethylhydrazine-induced colon tumors but reduces malignant invasion in mice en_US
dc.type Article en_US
dc.coverage.spacial United States en_US
dc.description.version peer reviewed en_US
dc.rights.holder Copyright © Routledge en_US

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