Role of the Catenin p120 in Breast Cancer
Abstract
Our working hypothesis is that induced p120 loss in the breast will impair E-cadherin function leading to (1) severe adverse consequences to lobular-alveolar development, and (2) positive effects on tumorigenesis or tumor progression leading to increased invasion and metastasis. To determine the role of p120 inactivation in breast cancer, we have proposed to study the consequences of targeted p120 loss of function in the mammary glands of normal and transgenic mouse models for tumorigenesis and metastasis. The first aim proposes to use gene targeting to incorporate loxp sites at strategic locations in the p120 gene such that Ore recombinase-induced deletion of the intervening sequence will inactivate p120. Mice containing this conditional allele (p120flox) will be generated and crossed with WAP-Cre mice to target the conditional deletion to the breast. Our major progress in this reporting period is successful testing of the Ore-induced recombination event in the targeting construct, and the generation of 397 ES cell lines, some of which appear to be expressing the homologously recombined floxed p120 allele. Thus, we anticipate successful generation of the p120 knockout mouse in the next six months. The mouse will be invaluable for studying further the role of p120 in metastasis and breast cancer.
Document Details
- Document Type
- Technical Report
- Publication Date
- Sep 01, 2001
- Accession Number
- ADA403615
Entities
People
- Albert B. Reynolds
Organizations
- Vanderbilt University Medical Center