Browse by author
Lookup NU author(s): Jessie Jeyapalan,
Dr Gabriele Saretzki,
Dr Michael Tilby,
Professor Thomas von Zglinicki
Full text for this publication is not currently held within this repository. Alternative links are provided below where available.
Cisplatin is a major chemotherapeutic agent, especially for the treatment of neuroblastoma. Telomeres with their sequence (TTAGGG)n are probable targets for cisplatin intrastrand cross-linking, but the role of telomeres in mediating cisplatin cytotoxicity is not clear. After exposure to cisplatin as single dose or continuous treatment, we found no loss of telomeres in either SHSY5Y neuroblastoma cells (telomere length, ∼4 kbp), HeLa 229 cells (telomere length, 20 kbp) or in the acute lymphoblastic T cell line 1301 (telomere length, ∼80 kbp). There was no induction of telomeric single strand breaks, telomeric overhangs were not degraded and telomerase activity was down-regulated only after massive onset of apoptosis. In contrast, cisplatin induced a delayed formation of DNA strand breaks and induced DNA damage foci containing γ-H2A.X at nontelomeric sites. Interstitial DNA damage appears to be more important than telomere loss or telomeric damage as induce r of the signal pathway towards apoptosis and/or growth arrest in cisplatin-treated tumour cells. © 2005 Wiley-Liss, Inc.
Author(s): Jeyapalan, J., Saretzki, G., Leake, A., Tilby, M.J., Von Zglinicki, T.
Publication type: Article
Publication status: Published
Journal: International Journal of Cancer
Print publication date: 01/06/2006
ISSN (print): 0020-7136
ISSN (electronic): 1097-0215
PubMed id: 16381006
Altmetrics provided by Altmetric