Cancer Letters
Volume 227, Issue 1 , Pages 1-7, 8 September 2005

BRCA1 in breast and ovarian cancer predisposition

  • Blase Billack

      Affiliations

    • Department of Pharmaceutical Sciences, College of Pharmacy and Allied Health Professions, St John's University, Jamaica, NY 11439, USA
    • ,
  • Alvaro N.A. Monteiro

      Affiliations

    • H. Lee Moffitt Cancer Center & Research Institute, MRC 3 West, 12902 Magnolia Drive, Tampa, FL 33612, USA
    • Corresponding Author InformationCorresponding author. Tel.: +1 813 745 6321; fax: +1 813 745 1720.

Received 25 October 2004; accepted 1 November 2004.

Abstract 

Women carrying one mutated BRCA1 allele are at increased risk of developing breast and ovarian cancer but tumor initiation requires the loss of the wild-type allele indicating that it is a tumor suppressor gene. In the 10 years since the cloning of BRCA1, a function for the gene product in the DNA damage response has been established. However, identifying the exact biochemical activities of BRCA1 has been a more difficult task. Our current understanding suggests that the molecular functions mediated by the terminal ends of BRCA1, which include an E3 ubiquitin ligase activity at the N-terminus and a protein–protein interaction surface at the C-terminus, are critical to the function of this protein in the response to DNA damage.

Keywords: BRCA1, Breast cancer, DNA damage, Ubiquitination, BRCT domain

Abbreviations: NPM, nucleophosmin/B23, siRNA, small interfering RNA

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PII: S0304-3835(04)00864-X

doi:10.1016/j.canlet.2004.11.006

Cancer Letters
Volume 227, Issue 1 , Pages 1-7, 8 September 2005

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