Mutation ofthe p53tumor-suppressor gene is recognized as one of the most common genetic alterations in human malignancy to date (1 ). Approximately 60% of human tumors are thought to possess mutation at thep53locus. Transient overexpression of the wild-typep53gene in various malignancies has been considered a potential molecular intervention strategy (2-7). This strategy is based on the role that wild-typep53plays as a tumor-suppressor gene and inducer of cell-cycle arrest and apoptosis (1,8-11).
