Inducing senescence, a permanent arrest of cell growth, in aged cells may be sufficient to guard against spontaneous cancer development, researchers discovered. By activating the senescence pathway in mice that can’t initiate apoptosis, researchers suceeded in suppressing spontaneous tumorigenesis.
Sandy Chang, assistant professor at M. D. Anderson’s department of cancer genetics and colleagues studied mice with dysfunctional telomeres that promote tumorigenesis in the absence of the tumor suppressor p53. The mice also had copies of the p53 gene that cannot initiate p53-dependent apoptosis but can execute p53-mediated senescence.
The authors found that activating the senescence pathway was sufficient to suppress spontaneous tumorigenesis. The team believes that thier findings suggest that by halting cellular proliferation, p53-mediated senescence may act as an important tumor suppressor mechanism in aged cells.
The paper is published online in EMBO reports.