Fanconi anemia (FA) is a fatal inherited disease displaying chromosomal 
instability, disturbances in oxygen metabolism and a high burden of 
intracellular radical oxygen species. Oxygen radicals can damage DNA including 
telomeric regions. Insufficient repair results in single strand breaks that can 
induce accelerated telomere shortening. In a longitudinal study we demonstrate 
that telomeric DNA is continuously lost at a higher rate in FA fibroblasts 
compared to healthy controls. Furthermore, we show that this loss is caused 
rather by an increased shortening per cell division in regularly replicating 
cells than by apoptosis.