The progression from normal breast epithelium to metastatic breast cancer is a complex, multistep process. Initially, genetic alterations are thought to confer a growth advantage to individual cells by decreasing tumor-suppressor gene activity or increasing oncogene activity, or both. Further alterations result in the development of cell clones that have the ability to invade adjacent tissue, establish metastatic deposits, and evade immune surveillance. At some point in this process, these malignant cell clones also lose the normal ability to respond to hormonal growth regulatory signals. Recent advances in understanding the genetic alterations, the loss of normal growth regulation, and the development of metastatic potential in breast cancer are reviewed. Factors related to the immunobiology of breast cancer are also discussed.