Because both properties characterize the tumor suppressor gene p53, the gene has emerged as one of the top targets in the war against cancer. P53 plays an integral role in activating programmed cell death (apoptosis) and is mutated in about 55 percent of tumor types. Potential relief strategies under development include replacing the defective gene, injecting viruses into tumors, and reactivating the gene's apoptotic function with small molecules.
When Arnold J. Levine, now president of Rockefeller University, and Princeton colleague Daniel I.H. Linzer discovered p53 in 1979, they had no conception that their finding would result in any of these approaches.1 By 1989, they suspected a tumor suppressor role,2 which Bert Vogelstein and colleagues at Johns Hopkins confirmed.3 And in 1994, researchers learned how the tumor suppressor interacted with downstream protein Mdm2 to turn the tumor suppressor function on and off.4 Fifteen years after its characterization, p53 had become a ...
