DNA Breakages Speed Telomere Shortening

By analyzing cells from a genetic syndrome called Fanconi's anemia, researchers at the Universitat Autonoma de Barcelona (Spain) found that breakages in the telomeric DNA sequence lead to accelerated telomere shortening. Their findings were reported in the February 15, 2002, issue of Human Molecular Genetics.

Fanconi's anemia is a genetic syndrome characterized by a high genetic instability and chromosomal fragility. It causes a very high predisposition to cancer in those who harbor the syndrome, such as a risk of leukemia that is 15,000 times higher than that of a healthy person. The researchers found that the telomeres of patients with Fanconi's anemia showed an accelerated shortening, owing to breakages in their DNA sequence, which resulted in chromosomes being unprotected and joining together. This mechanism may explain the tendency of these patients to contract cancer.

The research provides the first experimental link between a predisposition to cancer and the mechanism of sudden shortening of telomeres. Telomeres are very important to the genetic integrity of cells. Ordinarily, they prevent the chromosomes from joining together, protect their ends from degradation, and are involved in segregating chromosomes properly during cell division. Telomeres gradually shorten, which then indicates the point at which the cell dies.




Related Links:
Univ. Autonoma of Barcelona
Human Molecular Genetics