Linked Life Data

21097531

Source:http://linkedlifedata.com/resource/pubmed/id/21097531

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2011-3-3
pubmed:abstractText
Zinc deficiency is associated with high incidences of esophageal and other cancers in humans and leads to a highly proliferative hyperplastic condition in the upper gastrointestinal tract in laboratory rodents. Zn replenishment reduces the incidence of lingual, esophageal and forestomach tumors in Zn-deficient rats and mice. While previous animal studies focused on Zn deficiency, we have investigated the effect of Zn supplementation on carcinogenesis in Zn-sufficient mice of wild-type and tumor suppressor-deficient mouse strains. All mice received N-nitrosomethylbenzylamine and half the mice of each strain then received Zn supplementation. At killing, mice without Zn supplementation had developed more tumors than Zn-supplemented mice: wild-type C57BL/6 mice developed an average of 7.0 versus 5.0 tumors for Zn supplemented (P < 0.05); Zn-supplemented Fhit-/- mice averaged 5.7 versus 8.0 for control mice (P < 0.01); Zn-supplemented Fhit-/-Nit1-/- mice averaged 5.4 versus 9.2 for control mice (P < 0.01) and Zn-supplemented Fhit-/-Rassf1a-/- (the murine gene) mice averaged 5.9 versus 9.1 for control mice (P < 0.01). Zn supplementation reduced tumor burdens by 28% (wild-type) to 42% (Fhit-/-Nit1-/-). Histological analysis of forestomach tissues also showed significant decreases in severity of preneoplastic and neoplastic lesions in Zn-supplemented cohorts of each mouse strain. Thus, Zn supplementation significantly reduced tumor burdens in mice with multiple tumor suppressor deficiencies. When Zn supplementation was begun at 7 weeks after the final carcinogen dose, the reduction in tumor burden was the same as observed when supplementation began immediately after carcinogen dosing, suggesting that Zn supplementation may affect tumor progression rather than tumor initiation.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
1460-2180
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
32
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
351-8
pubmed:meshHeading
pubmed-meshheading:21097531-Acid Anhydride Hydrolases, pubmed-meshheading:21097531-Aminohydrolases, pubmed-meshheading:21097531-Animals, pubmed-meshheading:21097531-Blotting, Western, pubmed-meshheading:21097531-Carcinogens, pubmed-meshheading:21097531-Carcinoma, Squamous Cell, pubmed-meshheading:21097531-Dietary Supplements, pubmed-meshheading:21097531-Dimethylnitrosamine, pubmed-meshheading:21097531-Disease Progression, pubmed-meshheading:21097531-Immunoenzyme Techniques, pubmed-meshheading:21097531-Male, pubmed-meshheading:21097531-Mice, pubmed-meshheading:21097531-Mice, Inbred C57BL, pubmed-meshheading:21097531-Mice, Knockout, pubmed-meshheading:21097531-Neoplasm Proteins, pubmed-meshheading:21097531-Stomach Neoplasms, pubmed-meshheading:21097531-Tumor Suppressor Proteins, pubmed-meshheading:21097531-Zinc Compounds
pubmed:year
2011
pubmed:articleTitle
Effect of zinc supplementation on N-nitrosomethylbenzylamine-induced forestomach tumor development and progression in tumor suppressor-deficient mouse strains.
pubmed:affiliation
Department of Molecular Virology, Immunology and Medical Genetics, The Ohio State University Comprehensive Cancer Center, Columbus, OH 43210, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural