Non-Classical NF-kappaB Forms and Bcl-3 in Breast Cancer Development and Resistance to Cancer Therapy
Abstract
Breast cancer development typified by the overexpression of growth factors and growth factor receptors, expression of cell cycle markers such as cyclin Dl and c-myc, expression of chemokines such as RANTES, and development of resistance to cancer therapies. We and others have provided evidence that the transcription factor NF-kappa B and associated activities are expressed/activated in human breast cancer. Specifically we found that the NF-kB2/p52 NF-kappa B subunit and Bcl-3 are expressed in a significant number of breast tumors. Our preliminary data indicate that Bcl-3 expressing cells exhibit upregulation of cyclin Dl, c-myc, and the chemokine RANTES and that it leads to the strong suppression of the ability of Taxol to induce cell death. Our goals are to: (i) identify genes regulated by Bcl-3 that may be relavent to the progression of the disease, (ii) determine the mechanism whereby Bcl-3 blocks cancer-therapy induce apoptosis, and (iii) determine if Bcl-3 and the associated NF-kappa B subunit p52 are required for the development of experimental breast tumors in animal models. These goals may provide significant new insight into breast cancer progression and treatment.
Document Details
- Document Type
- Technical Report
- Publication Date
- Jun 01, 2004
- Accession Number
- ADA433238
Entities
People
- Albert S Baldwin
Organizations
- University of North Carolina at Chapel Hill