Preventing Cancer without Harming Cells

Initiating senescence in aged cells may be enough to protect against spontaneous cancer development, according to new research.

It was previously unknown whether cellular senescence or programmed cell death (apoptosis) was the more critical safeguard mechanism for suppressing tumors arising from dysfunctional telomeres. Aged cells have abnormal chromosomes with dysfunctional telomeres (shorter ends) that can induce tumorigenesis in the absence of the tumor suppressor p53, and may be related to the higher rate of cancer in older individuals. However, in the presence of p53, dysfunctional telomeres can induce a permanent arrest of cell growth, known as senescence.

Dr. Sandy Chang and colleagues, from M.D. Anderson Cancer Center (Houston, TX, USA), examined mutant mice with dysfunctional telomeres and copies of the p53 gene that cannot initiate p53-dependent apoptosis but can carry out p53-mediated senescence.

The investigators discovered that triggering the senescence pathway was sufficient to suppress spontaneous tumorigenesis. Their findings suggest that, by stopping cellular proliferation, p53-mediated senescence may act as an important tumor suppressor mechanism in aged cells.
The study was published online March 30, 2007, in the journal EMBO (European Molecular Biology Organization).


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M.D. Anderson Cancer Center