The problem is that the gene that has the instructions for making p53 occasionally mutates, which stops the protein’s activity. Once this happens, cancer-causing genes (known as oncogenes) take over the cell and set it free to divide uncontrollably, which is the very definition of cancer.
Mutations of the p53 gene, which is designated TP53, are also typified by more aggressive cancers, resistance to treatment by radiation and chemotherapy, and decreased patient survival. TP53 is “the most mutated gene in human cancer, and these mutations are correlated with more than 50 percent of all human cancer,” said Ronen Marmorstein, an authority on gene regulation at the Wistar Institute in West Philadelphia, Pa.
Scientists have developed drugs to repair the damaged p53 gene in mice, but so far they are still unavailable for humans. “The growing number of p53-targeting strategies raises hope for more efficient cancer therapies in the future,” wrote Swedish researcher Klas Wiman in the journal Cell Death and Differentiation.
In one experiment, for example, Gerard Evan, a researcher at the University of California’s Comprehensive Cancer Center in San Francisco, restored damaged p53 in mice suffering from lymphoma. “The tumors were completely dead within hours,” Evan said. “This result is very good news to the many of us who are thinking about trying to restore p53 function in established human cancers.”
The downside to restoring p53 function is that it may cause faster aging, at least in mice. “Cancer and senescence may be seen as two alternative fates in aging organisms, the secret of longevity being to find the best possible trade-off between these two options,” one scientist reported.