Background
Inherited mutations in BRCA2 are associated with a predisposition to early-onset breast cancers. The underlying basis of tumourigenesis is thought to be linked to defects in DNA double-strand break repair by homologous recombination (HR), as indicated by the spontaneous chromosomal instability phenotype of BRCA2-defective cell lines. The BRCA2 protein interacts with ssDNA and the RAD51 recombination protein, and is proposed to recruit RAD51 to the damage site for the HR repair.