Identification of Potential Therapeutc Mechanisms for HIP1 Inhibition in Breast Cancer
Abstract
The first hypothesis we proposed to the DOD was that HIP1 expression is necessary the breast cancer evolution. To test this we generated a cohort of breast cancer prone transgenic mice (MMTV-Myc) that are deficient (n=20) or replete for HIP1 (n=20). Our preliminary data indicates that HIP1 deficiency inhibits the progression of breast tumors in this mouse model. This is similar to our recently published work showing that HIP1 is necessary for the progression of prostate cancer (Bradley et al., 2005 Ca Res). These MMTV-Myc experiments are ongoing and we expect to have results on this first cohort of mice available for report at the Era of Hope meeting in June of this year. The second hypothesis we proposed to the DOD was that dysregulation of endocytosis of EGFR by HIP1 is a mechanism by which HIP1 promotes breast cancer evolution. Indeed, we have found that HIP1 overexpression inhibits the degradation the EGFR (Hyun et al., 2004 J Biol Chem). Showing that HIP1 is necessary for breast cancer progression and modulates key growth factor receptors involved in breast cancer, fuels the idea that HIP1 inhibition has excellent therapeutic potential. We will continue to explore the activity of HIP1 and search for inhibitors of HIP1 that may be useful in the treatment of breast cancer.
Document Details
- Document Type
- Technical Report
- Publication Date
- May 01, 2005
- Accession Number
- ADA436944
Entities
People
- Theodora S. Ross
Organizations
- University of Michigan