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 3p14.2, 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 is 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 past 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.

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Document Details

Document Type
Technical Report
Publication Date
Sep 01, 2004
Accession Number
ADA431696

Entities

People

  • Ya Wang

Organizations

  • Thomas Jefferson University

Tags

DTIC Thesaurus Topics

  • Abstracts
  • Biomedical Research
  • Biotechnology
  • Breast Cancer
  • Cell Line
  • Cell Physiological Processes
  • Cells
  • Culture Techniques
  • Data Science
  • Diseases And Disorders
  • Genes
  • Guidance
  • Ionizing Radiation
  • Materials
  • Neoplasms
  • Radiation
  • X Rays

Fields of Study

  • Biology

Readers

  • Molecular Biology and Genetics
  • Molecular and genetic basis of cancer.