Targeted disruption of Brca1 in restricted compartments of the mouse mammary epithelia

Tumours arising in BRCA1 mutation carriers have a characteristic phenotype, the molecular and cellular basis of which is unknown. To address the hypothesis that this phenotype reflects a role for BRCA1 in either in the basal or the stem cell compartments of the mammary epithelia, we have targeted it...

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Bibliographic Details
Published in:Breast cancer research and treatment 2008-11, Vol.112 (2), p.237-241
Main Authors: Smart, Chanel E., Clarke, Catherine, Brooks, Kelly M., Raghavendra, Ashwini, Brewster, Brooke L., French, Juliet D., Hetherington, Rehan, Fleming, Jean S., Rothnagel, Joseph A., Wainwright, Brandon, Lakhani, Sunil R., Brown, Melissa A.
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
BRCA1 Protein - chemistry
BRCA1 Protein - metabolism
Breast cancer
Cancer research
Cell Differentiation
Gene Deletion
Gene Expression Regulation, Neoplastic
Genes
Genes, BRCA1
Gynecology. Andrology. Obstetrics
Humans
Mammary gland diseases
Mammary Glands, Animal - metabolism
Medical sciences
Medicine
Medicine & Public Health
Mice
Mice, Knockout
Oncology
Phenotype
Preclinical Study
Promoter Regions, Genetic
Rodents
Stem Cells - metabolism
Transgenes
Tumors
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Summary:Tumours arising in BRCA1 mutation carriers have a characteristic phenotype, the molecular and cellular basis of which is unknown. To address the hypothesis that this phenotype reflects a role for BRCA1 in either in the basal or the stem cell compartments of the mammary epithelia, we have targeted its disruption to K14 and K6a expressing cells of the mouse. Unlike MMTV and WAP driven conditional knockout models of Brca1 , these two models did not result in any observable changes in the mammary gland. Our results suggest that BRCA1-associated tumours arise either in K14 and K6a negative basal cells of the mammary gland, or possibly from transdifferentiation of luminal epithelia.
ISSN:0167-6806
1573-7217
DOI:10.1007/s10549-007-9859-2