Multiple myeloma is a disease that despite a slow growth rate is considered resistant to standard chemotherapy. It is hypothesized that the tumor microenvironment contributes to the de novo drug resistance associated with the disease. This research will investigate the effects of adhesion of myeloma cells to fibronectin on the signaling pathways responsible for recognizing and ultimately repairing drug-induced DNA damage. Studies will be designed to address the effects of adhesion of myeloma cells to fibronectin on drug-induced DNA damage, and the subsequent elicitation of cell cycle checkpoints and DNA repair.