Heterozygous carriers for a BRCA2 mutation are highly susceptible of developing breast cancer. The BRCA2 protein is involved in regulating the DNA damage response and is important in maintaining genomic stability. Recent data has shown that cells lacking BRCA2 might suffer from replication problems at telomeric regions. The aim of the study is to use BRCA2 heterozygous cell lines and examine whether or not these cell lines are defective in the protection and stabilization of replication forks at telomeric regions. In addition, we have used the same cell lines to examine the DNA damage response by analyzing formation of gamma-H2AX and Rad51 foci in the presence or absence of PARP1 inhibitor. PARP1 is involved in DNA single-strand break repair and when inhibited those single strand breaks are converted to DNA double strand breaks during S phase. This allows us to examine the role of BRCA2 in the repair of DNA double strand breaks in cell lines heterozygous for BRCA2 mutation. Using a lentiviral system, we were able to knock down the remaining copy of BRCA2 within the heterozygous cell lines and therefore create a homozygous -/- version to compare with the heterozygous line.