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Salk Scientists - Links Between Cancer and Aging

ighly colorful variation of the FISH technique called chromosome painting. This technique 'paints' or labels every pair of the 46 chromosomes with a different colored fluorescent dye, enabling investigators to easily see breakage or fusion of chromosomes that are characteristic of damaged DNA under the microscope.

Then they artificially supplied the cultured cells with one of two genes-either a functional copy of the WRN gene, which is mutant or nonfunctional in Werner Syndrome, or a gene encoding the protein telomerase, which elongates short or missing telomeres. After cells divided several times, their DNA was reexamined for the type of damage associated with both aging and cancer.

Cells supplied with a functional WRN gene showed decreased DNA damage compared to untreated cells, which was predictable: the WRN gene encodes a protein called a helicase that unwinds tightly coiled DNA strands when cells divide. Loss of WRN protein in individuals with Werner Syndrome is responsible for the disease. Explains Crabbe, now a postdoctoral fellow at The Institute of Human Genetics in Montpellier, France, 'The lack of a single protein (WRN) induced loss of some telomeres, leading to a premature cellular growth arrest.'

However, the most interesting finding was what the scientists observed in cells supplied with added telomerase. 'When we put telomerase into cells, we suppressed accumulation of mutations to the same degree as when we put the WRN protein back,' reports Karlseder. 'It fixed the defect by elongating short telomeres seen in Werner Syndrome cells.'

Crabbe, who is continuing to study DNA replication as a postdoc, concludes that these findings not only provide a mechanism underlying accelerated aging seen in Werner Syndrome but establish a link to cancer predisposition, saying, 'These results indicate that the telomere dysfunction in Werner Syndrome cells is a major cause of genomic instability and could explain the high incid
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