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Mutation of the p53 tumor-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 the p53 locus. Transient overexpression of the wild-type p53 gene in various malignancies has been considered a potential molecular intervention strategy (2 -7). This strategy is based on the role that wild-type p53 plays as a tumor-suppressor gene and inducer of cell-cycle arrest and apoptosis (1 ,8-11).
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