Hormone Resistance and Progesterone Receptors in Breast Cancer.
Abstract
We postulate that breast cancers become "resistant" to hormone therapy because antagonists acquire inappropriate, agonist-like, effects. The clinical consequences of such a functional switch are grave. The studies we have proposed address the molecular mechanism by which antagonist-occupied progesterone B-receptors become transcriptional agonists. Purpose of Present Work: Aim 1. The functional differences between A and B-receptors in breast cancer cells. Aim 2. BUS - The B-upstream segment. A third transcriptional activation domain unique to B-receptors? Aim 3. Mechanisms of AF-3 action in the BUS segment.
Document Details
- Document Type
- Technical Report
- Publication Date
- Aug 01, 1996
- Accession Number
- ADA321147
Entities
People
- Kathryn B. Horwitz
Organizations
- University of Colorado Health