Effects of Herstatin an Alternative Her-2 (erbB-2) Product on Hormonal Responsiveness of Breast Cancer
Abstract
The establishment and progression of breast cancer is controlled by receptors for estrogens (ER) and peptide growth factors (1, 2, 3). Several lines of evidence suggest that estrogen responsiveness and resistance to anti-estrogens may be influenced by cross- talk between ER and erbB receptor pathways. Overexpression of HER-2 (erbB2) and signaling triggered by the erbB growth factor, Heregulin (HRG), has been found to confer resistance to the antiestrogen, tamoxifen (4-7). The involvement of erbB receptors has led to suggestions that receptor targeted inhibitors may enhance the therapeutic efficacy of tamoxifen. We recently discovered an alternative HER-2 product called Herstatin, which binds to HER-2 and the EUF receptor (EGFR) and blocks their activation (8-10). Preliminary studies indicate that Herstatin blocks both EUF and HRG signaling in estrogen responsive MCF7 cells and therefore may enhance tamoxifen sensitivity in breast cancer cells. Purpose: The objective of this proposal is to thoroughly evaluate the effects of Herstatin on hormonal responsiveness of ER positive breast cancer cells. Scope: The proposed research will evaluate the potential therapeutic efficacy of Herstatin combined with tamoxifen in the treatment of breast cancer.
Document Details
- Document Type
- Technical Report
- Publication Date
- Jun 01, 2004
- Accession Number
- ADA425743
Entities
People
- Gail M. Clinton
Organizations
- Oregon Health & Science University