Cas Signaling in Breast Cancer
Abstract
Resistance to antiestrogens is a serious clinical problem in breast cancer treatment, and a better understanding of the mechanisms of antiestrogen resistance is urgently needed. Our hypothesis, which is supported by our preliminary data, is that the signaling molecule Cas- has an important causal role in the development of antiestrogen resistance. As a corollary, understanding of the pathways that Cas activates may identify key regulators of antiestrogen resistance and novel targets for breast cancer treatment, and measurements of Cas signaling levels may provide useful prognostic information for breast cancer patients. Our objective is to test our hypothesis, and to identify the signaling pathways that mediate Cas-induced antiestrogen resistance. Our working model is that the Rac-JNK pathway forms a common pathway downstream of the Cas/Crk/BCAR3 signaling complex to mediate antiestrogen resistance. Testing this model relies on reciprocal analysis of dominant-negative and constitutively active forms of the various signaling molecules in this pathway. As such, bulk of our efforts during the first year have focused on generating the genetic and cellular tools described in the report in detail, allowing us to perform rigorous functional studies on the antiestrogen resistance in breast cancer cells during the upcoming year.
Document Details
- Document Type
- Technical Report
- Publication Date
- May 01, 2005
- Accession Number
- ADA435633
Entities
People
- Kristina Vuori
Organizations
- Sanford Burnham Prebys Medical Discovery Institute