Human cells can process DNA double-strand breaks (DSBs) by either homology 
directed or non-homologous repair pathways. Defects in components of DSB repair 
pathways are associated with a predisposition to cancer. The products of the 
BRCA1 and BRCA2 genes, which normally confer protection against breast cancer, 
are involved in homology-directed DSB repair. Defects in another 
homology-directed pathway, single-strand annealing, are associated with genome 
instability and cancer predisposition in the Nijmegen breakage syndrome and a 
radiation-sensitive ataxia-telangiectasia-like syndrome. Many DSB repair 
proteins also participate in the signaling pathways which underlie the cell's 
response to DSBs.