Cancer: Linking Breast Cancer and DNA Repair

Science's STKE  09 Nov 1999:
Vol. 1999, Issue 7, pp. tw8
DOI: 10.1126/stke.1999.7.tw8

Failure of cell cycle checkpoint mechanisms that prevent cell division in the presence of damaged DNA can lead to an accumulation of genetic errors and can contribute to formation of cancerous cells. Cortez et al. report that two proteins that are associated with increased risk of breast cancer in humans in their mutated form actually interact with one another in cells and function in the response to DNA damage. They provide evidence that Brca1 (for breast cancer gene 1) is a substrate for ATM (for mutated in ataxia telangiectasia), a protein kinase that is activated in cells with damaged DNA. Phosphorylation of Brca1 by ATM appears to be required for proper function of Brca1 in protecting cells from DNA damage.

Cortez, D., Wang, Y., Qin, J., and Elledge, S.J. (1999) Requirement of ATM-dependent phosphorylation of Brca1 in the DNA damage response to double-strand breaks. Science 286: 1162-1166. [Abstract] [Full Text]

Venkitaraman, A.K. (1999) Breast cancer genes and DNA repair. Science 286: 1100-1102. [Summary] [Full Text]