Telomeres, Cancer, and Immortality

Numerous genetic accidents, including the activation of proto-oncogenes and the loss of tumor-suppressor genes, can result in the stimulation of cell division. However, mammalian cells have evolved an intricate set of checks and balances against uncontrolled cellular proliferation. One of these is cellular suicide, or apoptosis, triggered by the p53 gene in the presence of aberrant growth signals. Another appears to be the progressive shortening of the ends of chromosomes, or telomeres, that accompanies normal cell division and may contribute to cellular aging. Support for this concept comes from a recent article in Science by Kim and coworkers,1 reporting a . . .