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Wednesday, 2 January, 2002, 18:43 GMT
The cost of warding off cancer
Cancer drugs may promote premature ageing
The natural defence mechanism that the body uses to fight cancer may come at a price.
Research suggests that it might also accelerate the ageing process. The finding raises the possibility that powerful drugs used to treat cancer may cause patients to age prematurely. The research, published in the journal Nature, centres on a protein called p53 which has been identified as playing a crucial role in preventing cancer. It does this blocking the uncontrolled cell division associated with the disease, repairing damaged genetic material and promoting cell death. Mice experiments Scientists led by Lawrence Donehower, at Baylor College of Medicine in Houston, Texas, boosted levels of p53 in genetically-modified mice. As expected, mutant mice with excess p53 developed far fewer cancer tumours than normal animals - but they did not live longer. In fact, their average lifespan was reduced by nearly 20% from 118 weeks to 96 weeks. Mice with extra p53 developed early signs of old age such as muscle loss, hunched backs, and brittle bones. Their wounds also took longer to heal. The researchers suspect that too much p53 stunts the division of stem cells which normally replenish tissues such as skin and bones in adults. It is the first time that p53 has been implicated in ageing. Side effect theory Two experts reviewing the work in Nature said it raised "the shocking possibility that ageing may be a side effect of the natural safeguards that protect us from cancer". Gerardo Ferbeyre, from the University of Montreal in Canada, and Scott Lowe, of the Cold Spring Harbor Laboratory in New York, said it was possible p53 contributed to premature ageing or age-related disorders in humans. It may even be one reason why different people have different lifespans, they suggested. There could also be worrying implications for the way cancer was treated. Ferbeyre and Lowe wrote: "The results also raise the disturbing possibility that the DNA-damaging drugs used to treat cancer in young people might prompt p53 into action and accelerate age-related disorders later on. "This is a testable hypothesis, and the prospect alone underscores the need for less toxic anti-cancer drugs."
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