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June 9, 2006
Cancer-aging link found
A report published in the June 2, 2006 issue of Science revealed the discovery that checkpoint proteins, which prevent the division of defective cells that can lead to cancer, are also involved in limiting life span. The finding reveals an important link between cancer and the increased risk of the disease that occurs with aging.
A research team led by Professor Gordon Lithgow, who started the project at the University of Manchester and completed it at the Buck Institute in California, genetically programmed the roundworm C. elegans to lack checkpoint proteins, which resulted in a 15 to 30 percent increase in the animal's life span.
"We have discovered that proteins that prevent cancer in humans by ensuring that cells don't divide if they are damaged also determine lifespan in the nematode worm," Dr Lithgow stated. "Our research has shown that these 'checkpoint proteins' – thought only to operate in cells that divide – function in cells that no longer divide as well. The fact that they appear to have dual functions opens a new way to study the connection between aging and cancer. If we look at checkpoint proteins as a gear, we have known for a long time that they drive the cancer engine; now we know that they also drive the longevity engine. This discovery has exciting potential as an area of inquiry into potential cellular links between aging and cancer."
Dr Dale Bredesen, who is the Buck Institute's Scientific Director, added, "If we're smart about it, we might be able to design strategies where you could keep checkpoint proteins active in dividing cells and stop them working in cells that no longer divide, such as brain cells. Increasing the survival of brain cells or 'neurons' could provide a new avenue of treatment for neurodegenerative diseases like Alzheimer's."
Cancer-aging link found
A report published in the June 2, 2006 issue of Science revealed the discovery that checkpoint proteins, which prevent the division of defective cells that can lead to cancer, are also involved in limiting life span. The finding reveals an important link between cancer and the increased risk of the disease that occurs with aging.
A research team led by Professor Gordon Lithgow, who started the project at the University of Manchester and completed it at the Buck Institute in California, genetically programmed the roundworm C. elegans to lack checkpoint proteins, which resulted in a 15 to 30 percent increase in the animal's life span.
"We have discovered that proteins that prevent cancer in humans by ensuring that cells don't divide if they are damaged also determine lifespan in the nematode worm," Dr Lithgow stated. "Our research has shown that these 'checkpoint proteins' – thought only to operate in cells that divide – function in cells that no longer divide as well. The fact that they appear to have dual functions opens a new way to study the connection between aging and cancer. If we look at checkpoint proteins as a gear, we have known for a long time that they drive the cancer engine; now we know that they also drive the longevity engine. This discovery has exciting potential as an area of inquiry into potential cellular links between aging and cancer."
Dr Dale Bredesen, who is the Buck Institute's Scientific Director, added, "If we're smart about it, we might be able to design strategies where you could keep checkpoint proteins active in dividing cells and stop them working in cells that no longer divide, such as brain cells. Increasing the survival of brain cells or 'neurons' could provide a new avenue of treatment for neurodegenerative diseases like Alzheimer's."
