Significance of ERa and c-Src Interaction in the Progression of Hormone Independent Breast Cancer
Abstract
We have shown previously that c-Src null epithelial cells are unable to respond to estrogenic stimulation [1]. In addition, c-Src recruitment to ErbB-2 catalytic domain could be involved in the hormone independent response of ErbB-2 induced mammary tumorigenesis [2]. In order to assess whether ablation of c-Src can influence the ability of mammary epithelial cells to respond to hormonal stimulation, we are currently generating a mouse strain homozygous for the loss of c-Src tyrosine kinase specifically in the mammary epithelium. We have also derived several independent mouse strains that express, under the control of an MMTV promoter, a chimeric EGF Receptor (TK) carrying the catalytic domain of ErbB-2 and thus able to recruit c-Src. Concomitantly, we have generated transgenic mice expressing wild-type EGFR under the transcriptional control of the MMTV promoter. Comparison of the mammary tumor incidence between these mouse strains will provide important insight into the importance of the recruitment of c-Src by ErbB-2 in hormone responsiveness of breast cancers.
Document Details
- Document Type
- Technical Report
- Publication Date
- Dec 01, 2005
- Accession Number
- ADA456013
Entities
People
- William Muller
Organizations
- McGill University