Nuclear proteins encoded by both cellular oncogenes and DNA tumor viruses enable activated ras oncogenes to transform a variety of cell types to a tumorigenic state. The interactions are complementary, suggesting that collaborating oncogenes release cells from controls that preclude transformation by ras alone. The nuclear oncoproteins bind both protein and nucleic acid targets and affect processes important in transcription and cell cycle control. Transforming collaborations between oncogenes provide a genetic context to study biochemical interactions involved in normal growth control and to identify mechanisms important in multistep carcinogenesis.