Genomic Instability and Breast Cancer
Abstract
Our breast cancer research program initially focused on tumor suppressor BRCA1. In the past few years, we elucidated how BRCA1 is regulated and participates in the maintenance of genomic stability. Our studies demonstrated that loss of BRCA1 function leads to cell cycle checkpoint and repair defects and thus contributes to the development of familial breast cancer. Recently, we expanded our research program beyond BRCA1 and DNA damage responsive pathways. We studied several other signal transduction pathways, which are equally important for the maintenance of genomic stability and cell proliferation. These include Chfr and mitotic checkpoint regulation, and DBC1 (Deleted in Breast Cancer 1) and its role in the regulation of SIRT1. Together these studies revealed how the deregulation or disruption of these pathways would lead to breast cancer development. Moreover, we initiated several largescale studies, which we hope will provide potential targets for the development of anticancer therapy.
Document Details
- Document Type
- Technical Report
- Publication Date
- Jun 01, 2011
- Accession Number
- ADA554776
Entities
People
- Junjie Chen
Organizations
- The University of Texas MD Anderson Cancer Center