Linked Life Data

16111884

Source:http://linkedlifedata.com/resource/pubmed/id/16111884

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
2005-11-4
pubmed:abstractText
The Vitamin D receptor (VDR) and its ligand, 1,25(OH)(2)D(3), regulate cell proliferation, differentiation and apoptosis in vitro, yet the physiological significance of this regulation is unclear. In these studies, we used VDR knockout (VDRKO) mice to examine the impact of VDR on chemical carcinogen-induced tumorigenesis in vivo. Wild type (WT) and VDRKO littermates were fed a high calcium diet to prevent disturbances in calcium homeostasis and were gavaged with dimethylbenzanthracence (DMBA) using a protocol designed to induce mammary tumors. Compared to WT littermates, VDRKO mice exhibited an increased incidence of mammary gland hyperplasia and a higher percentage of hormone independent tumors with squamous differentiation. VDR ablation also significantly enhanced tumor development in epidermis and lymphoid tissues, but did not affect tumor development in ovary, uterus, lung or liver. These data indicate that VDR ablation alters susceptibility to DMBA-induced carcinogenesis in a tissue specific fashion, and provide support that optimal VDR signaling may act to suppress tumorigenesis.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0960-0760
pubmed:author
pubmed:issnType
Print
pubmed:volume
97
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
153-64
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
2005
pubmed:articleTitle
Vitamin D receptor (VDR) ablation alters carcinogen-induced tumorigenesis in mammary gland, epidermis and lymphoid tissues.
pubmed:affiliation
Department of Biological Sciences, University of Notre Dame, 214 Galvin Life Sciences Building, Notre Dame, IN 46556, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural