Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2007;12(2):192-205.
doi: 10.2478/s11658-006-0063-x. Epub 2006 Dec 18.

Genetic instability in the RAD51 and BRCA1 regions in breast cancer

Affiliations

Genetic instability in the RAD51 and BRCA1 regions in breast cancer

Maria Nowacka-Zawisza et al. Cell Mol Biol Lett. 2007.

Abstract

Breast cancer is the most prevalent cancer type in women. Accumulating evidence indicates that the fidelity of double-strand break repair in response to DNA damage is an important step in mammary neoplasias. The RAD51 and BRCA1 proteins are involved in the repair of double-strand DNA breaks by homologous recombination. In this study, we evaluated loss of heterozygosity (LOH) in the RAD51 and BRCA1 regions, and their association with breast cancer. The polymorphic markers D15S118, D15S214 and D15S1006 were the focus for RAD51, and D17S855 and D17S1323 for BRCA1. Genomic deletion detected by allelic loss varied according to the regions tested, and ranged from 29 to 46% of informative cases for the RAD51 region and from 38 to 42% of informative cases for the BRCA1 region. 25% of breast cancer cases displayed LOH for at least one studied marker in the RAD51 region exclusively. On the other hand, 31% of breast cancer cases manifested LOH for at least one microsatellite marker concomitantly in the RAD51 and BRCA1 regions. LOH in the RAD51 region, similarly as in the BRCA1 region, appeared to correlate with steroid receptor status. The obtained results indicate that alteration in the RAD51 region may contribute to the disturbances of DNA repair involving RAD51 and BRCA1 and thus enhance the risk of breast cancer development.

PubMed Disclaimer

Similar articles

Cited by

References

    1. Nathanson K.L., Weber B.L. "Other" breast cancer susceptibility genes: searching for more holy grail. Hum. Mol. Genet. 2001;10:715–720. doi: 10.1093/hmg/10.7.715. - DOI - PubMed
    1. Welcsh P.L., King M.C. BRCA1 and BRCA2 and the genetics of breast and ovarian cancer. Hum. Mol. Genet. 2001;10:705–713. doi: 10.1093/hmg/10.7.705. - DOI - PubMed
    1. Auranen A., Song H., Waterfall C., Dicioccio R.A., Kuschel B., Kjaer S.K., Hogdall E., Hogdall C., Stratton J., Whittemore A.S., Easton D.F., Ponder B.A., Novik K.L., Dunning A.M., Gayther S., Pharoah P.D. Polymorphisms in DNA repair genes and epithelial ovarian cancer risk. Int. J. Cancer. 2005;117:611–618. doi: 10.1002/ijc.21047. - DOI - PubMed
    1. Cousineau I., Abaji C., Belmaaza A. BRCA1 regulates RAD51 function in response to DNA damage and suppresses spontaneous sister chromatid replication slippage: implications for sister chromatid cohesion, genome stability, and carcinogenesis. Cancer Res. 2005;65:11384–11391. doi: 10.1158/0008-5472.CAN-05-2156. - DOI - PubMed
    1. Schmutte C., Tombline G., Rhiem K., Sadoff M.M., Schmutzler R., von Deimling A., Fishel R. Characterization of the human Rad51 genomic locus and examination of tumors with 15q14-15 loss of heterozygosity (LOH) Cancer Res. 1999;59:4564–4569. - PubMed

Publication types