Linked Life Data

11181458

Source:http://linkedlifedata.com/resource/pubmed/id/11181458

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2001-2-22
pubmed:abstractText
The proteins encoded by BRCA1 and ATM may be important in DNA repair and maintenance of genomic integrity. Women heterozygous for a mutation in BRCA1 have an increased incidence of breast cancer. Some evidence also suggests that female carriers of ATM mutations may be susceptible to breast cancer. However, mice carrying one mutant allele of Brca1 or ATM are not highly susceptible to breast cancer. We proposed that heterozygosity for a mutant allele of Brca1 or ATM may confer a decreased ability to repair DNA damage. Such a defect might lead to a heightened sensitivity to tumor development in susceptible animal models. Therefore, mice predispose to mammary tumor development might show an increased susceptibility if they also carry an ATM or Brca1 mutation. C57BL/6J (B6) MIN/+ mice are predisposed to mammary and intestinal tumors and exposure to the point mutagen ethylnitrosourea (ENU) markedly increases mammary tumor multiplicity and incidence. To test our hypothesis, B6.MIN/+ male mice were crossed with 129S6/SvEvTac females heterozygous for a mutant allele of either Brca1 or ATM. Female progeny from each cross were treated with ENU and followed for tumor development. Only MIN/+ F1 females developed mammary tumors and heterozygosity for a mutant Brca1 or ATM allele had no effect on mammary or intestinal tumor incidence and multiplicity. These results suggest that heterozygosity for a mutation in Brca1 or ATM: does not affect MIN-induced tumorigenesis in mice under these conditions. Additionally, exposure to a somatic point mutagen does not increase tumor development in mice carrying Brca1 or ATM mutations.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0143-3334
pubmed:author
pubmed:issnType
Print
pubmed:volume
22
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
343-6
pubmed:dateRevised
2011-11-2
pubmed:meshHeading
pubmed-meshheading:11181458-Animals, pubmed-meshheading:11181458-Cell Cycle Proteins, pubmed-meshheading:11181458-DNA Primers, pubmed-meshheading:11181458-DNA-Binding Proteins, pubmed-meshheading:11181458-Ethylnitrosourea, pubmed-meshheading:11181458-Female, pubmed-meshheading:11181458-Genes, BRCA1, pubmed-meshheading:11181458-Genetic Predisposition to Disease, pubmed-meshheading:11181458-Incidence, pubmed-meshheading:11181458-Loss of Heterozygosity, pubmed-meshheading:11181458-Mammary Neoplasms, Experimental, pubmed-meshheading:11181458-Mice, pubmed-meshheading:11181458-Mice, Knockout, pubmed-meshheading:11181458-Mutation, pubmed-meshheading:11181458-Phenotype, pubmed-meshheading:11181458-Polymerase Chain Reaction, pubmed-meshheading:11181458-Protein-Serine-Threonine Kinases, pubmed-meshheading:11181458-Tumor Suppressor Proteins
pubmed:year
2001
pubmed:articleTitle
Heterozygosity for a mutation in Brca1 or Atm does not increase susceptibility to ENU-induced mammary tumors in Apc(Min)/+ mice.
pubmed:affiliation
Laboratory of Genetics and Department of Human Oncology, University of Wisconsin-Madison, Madison, WI 53792, Genetic Disease Research Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD , USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't