Chromosome instability (left) is not a problem for cells with a p53 point mutation (right).

Lozano/Macmillan

Vvertebrate p53 has many talents, including the ability to induce apoptosis and cell cycle arrest in response to DNA damage. At least one of these talents seems to be crucial for suppressing tumor formation, as mice that lack p53 develop early onset T-cell lymphomas and usually die young. New results from Geng Liu, Guillermina Lozano, and colleagues (M.D. Anderson Cancer Center, Houston, Texas) suggest that, for tumor initiation, delay trumps death.

The group made mice with a p53 point mutation that leaves the protein with the ability to delay cell cycle but not induce apoptosis. This mutation causes a much less severe phenotype than p53 deletions, with a long delay in tumor onset and only rare cases of lymphoma. They then showed that the decreased tumorigenesis is a result...

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