Too much of a cancer-preventing protein leads to premature ageing in mice, researchers have found in the 03 Jan 02 issue of Nature (Vol. 415, No. 6867, 03 Jan 2002). The result suggests that the body may have to strike a balance between preventing cancer and succumbing to old age.
Lawrence Donehower of Baylor College of Medicine, Houston, and colleagues created mutant mice in which the p53 protein is hyperactivated. p53 is one of the cell's key lines of defence, halting cell division, repairing DNA damage and triggering cell death.
As expected, the mice developed far fewer tumours than their normal counterparts, but they did not live longer. Their average lifespan was 96 weeks, compared with 118 weeks for normal mice — a reduction of nearly 20%. The symptoms of the mutant mice included weight and muscle loss, hunched backs and brittle bones, and their wounds took longer to heal.
This is the first time that p53 has been implicated in ageing. The team suspect the excess p53 stunts the division of stem cells that normally replenish tissues such as skin and bone in adults.
"These results raise the disturbing possibility that the genotoxic agents used to treat cancer in young individuals might accelerate age-related disorders later on," suggest Gerardo Ferbeyre of the Université de Montréal, Canada, and Scott W. Lowe of Cold Spring Harbor Laboratory, New York, in an accompanying News and Views article about the background and implications of this work.
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(C) Nature press release.
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