title: Accelerated telomere shortening in Fanconi anemia fibroblasts--a longitudinal study.
abstract: 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.
authors.affiliation: Institute of Biochemistry, Free University Berlin, Germany.
authors.forename: C
authors.initials: C
authors.lastname: Adelfalk
authors.forename: M
authors.initials: M
authors.lastname: Lorenz
authors.forename: V
authors.initials: V
authors.lastname: Serra
authors.forename: T
authors.initials: T
authors.lastname: von Zglinicki
authors.forename: M
authors.initials: M
authors.lastname: Hirsch-Kauffmann
authors.forename: M
authors.initials: M
authors.lastname: Schweiger
mesh_terms: D000293:Adolescent; D000328:Adult; D017209:Apoptosis; D002455:Cell Division; D002460:Cell Line; D002648:Child; D004249:DNA Damage; D005199:Fanconi Anemia / Q000235:genetics* / Q000473:pathology; D005260:Female; D006801:Humans; D007223:Infant; D008137:Longitudinal Studies; D008297:Male; D018384:Oxidative Stress; D016615:Telomere