Stability of the genetic material is critical for all organisms including human beings. Exposure to radioactivity adversely affects genome stability by causing random breaks in the DNA backbone, leading to cell death. In humans, such breaks are predominantly repaired by an enzyme, DNA Ligase IV, via a random non-homologous end joining process. Thus, Ligase IV plays an important role in maintaining genetic stability. As a result, Ligase IV also makes it harder to treat cancer by inducing double stranded DNA breaks. Understanding the role of DNA ligase IV in cancer cells is critical to developing effective treatments. This project will study the effects that DNA damage has on the levels of Ligase IV in human cancer cell. The lines HTB-19, HTB-20, and HTB-26 will be used as model cells for this project. These cells will be treated with varying concentrations of radiomimetic drugs (compounds that mimic the effect of radiation by initiating DNA double-strand breakage). After the treatment the level and function of Ligase IV will be analyzed with respect to cell viability.