A New Therapeutic Paradigm for Breast Cancer Exploiting Low Dose Estrogen-Induce Apoptosis
Abstract
To discover the mechanism of estrogen induced breast cancer cell apoptosis and establish the clinical value of short-term low dose estrogen treatment to cause apoptosis in antihormone resistance breast cancer. To achieve the goal, we have created an optimal collaborative network to study laboratory models of the regulation of estrogen-induced growth and apoptosis in breast cancer. The molecular mechanisms of estrogen action (ER) mediated regulation are being deciphered by the systematic distribution of processed tissues from the Fox Chase Cancer Center (FCCC) to Translational Genomics (TGen) for genomics (siRNA analysis, CGH, and Agilent gene array) and to Georgetown University (GU) for proteomic analysis. All derived data is being loaded on a secure website for analysis. A complimentary clinical trial is currently recruiting to evaluate the antitumor effects of high dose estradiol (30 mg daily) in patients following the success and failure of two consecutive antihormonal therapies. We have published our findings about a new secreted protein, CEACAM-6 in estrogen-deprived breast cancer cells that enhances tumor invasion. We report our studies of the regulation of the antiapoptotic protein Bcl-2 by the estrogen induced protein XBP-1. This protein is overexpressed in our antihormone resistant cell lines as is Bcl-2.
Document Details
- Document Type
- Technical Report
- Publication Date
- Sep 01, 2008
- Accession Number
- ADA626322
Entities
People
- Virgil C. Jordan
Organizations
- Fox Chase Cancer Center