Mechanism Controlling DNA Damage Response Has Potential Novel Medical Applicatio

Previously, the rise in the level of p53 in cells whose DNA had been damaged was thought to be due only to a decrease in the rate at which the p53 protein is broken down in the cell. The St. Jude study showed that the level of p53 protein synthesis increases following DNA damage. This discovery suggests that scientists can use this newly recognized mechanism to modulate p53 function in the cell in order to control whether cells in the body mutate, and whether cells live or die after DNA damage. A report on this work appears in the October 7 issue of the journal Cell.

If a cell has been damaged, p53 protects the body by either preventing that cell from dividing or triggering a cascade of molecular signals that causes that cell to commit suicide—a process called apoptosis. In this way, p53 rids the body of useless cells and prevents cells with potentially cancer-causing mutations from multiplying and spreading. Failure of a cell to activate p53 function after DNA damage can contribute to the generation of genetically altered cells that leads to cancer.

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