A New Explanation for the Roles of Fhit Protein in the Progress of Breast Cancer
Abstract
Alteration of the Fragile Histidine Triad (FHIT) gene, encompassing the FRA3B fragile site at chromosome 3pl4.2, especially reduction or deletion of its expression, is involved in many breast cancers. Little is known about the biological function of the Fhit in breast cancer progression. The major goal of this proposal is to test the hypothesis that the over-activated ATR pathway in irradiated Fhit* cells promote the homologous recombination repair (HRR) of DNA DSBs, resulting in more Fhit* cells surviving with deletion or translocations at fragile sites (malignant feature). In the passed year with this grant support, we found that the over-activated ATR pathway regulated checkpoint contributes the radioresistance of Fhit* cells and ATR is linked to HRR but not non-homologue end joining repair. These results will provide theory guidance for improving clinical treatment of breast cancers in which Fhit is deleted or reduced by combining traditional therapy with blocking the ATR pathway.
Document Details
- Document Type
- Technical Report
- Publication Date
- Sep 01, 2005
- Accession Number
- ADA443827
Entities
People
- Ya Wang
Organizations
- Thomas Jefferson University