Among many forms of DNA damage, DNA double strand breaks (DSBs) are considered to be most dangerous and unrepaired or misrepaired DSBs causes genomic instability and cancer. Thus, maintenance of genomic integrity is of fundamental importance and organisms have developed genome surveillance mechanisms to activate DNA damage response network. This response controls various cellular processes including checkpoint activation, DNA repair and apoptosis. Homologous recombination (HR) plays an important role in the maintenance of genome integrity by repairing endogenous and exogenous DSBs. Several tumor suppressor genes such as hereditary breast and ovarian cancer susceptibility BRCA1 and BRCA2 genes, the Bloom syndrome gene (BLM) and Fanconi anemia genes (FA) have been shown to regulate HR. In addition, the products of DNA damage activated ATM and ATR genes and the Nijmegen breakage syndrome gene (NBS1) and the MRE11 also regulate HR. Our lab is interested in understanding the molecular mechanism(s) of DNA damage response, HR mediated DSB repair and chromosome instability associated with genetic diseases and cancer.