A Mouse Model to Investigate the Role of DBC2 in Breast Cancer
Abstract
Hereditary breast cancer is frequently due to a germline heterozygous mutation of either Brca1 or Brac2. However, familial breast cancer accounts for only a small minority of breast cancer cases. Sporadic breast cancer, on the other hand, represents 90% of breast cancer patients. Mutations of both oncogenes and tumor suppressor genes often occur in spontaneous breast cancer. Specifically, tumor suppressor gene activity may be abrogated or decreased in cancer cells. Recently, a putative tumor suppressor gene, DBC2(Deleted in Breast Cancer), was discovered that appears to be frequently mutated in sporadic breast cancer. DBC2 expression cannot be detected in half of the spontaneous breast cancer tissues and cells tested and 2) wild-type (WT) DBC2 expressed in a breast cancer cell line, T47D, inhibited cellular proliferation while mutated DBC2 expression did not repress growth of the breast cancer cells. These data imply that mutation of DBC2 is important for the development of spontaneous breast cancer. This proposal serves to investigate the functional role of DBC2 in cells and mice to elucidate the function of DBC2 for tumor suppression. To this end, we have generated embryonic stem cells heterozygous for DBC2 to execute these studies.
Document Details
- Document Type
- Technical Report
- Publication Date
- Mar 01, 2005
- Accession Number
- ADA434065
Entities
People
- Valerie Boka
Organizations
- University of Texas Health Science Center at San Antonio