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Association of Mutant TP53 with Alternative Lengthening of Telomeres and Favorable Prognosis in Glioma

¹ Department of Pathology, University of Otago; ² Dunedin Public Hospital, Dunedin, New Zealand; ³ Institute for Cancer Studies, Division of Genomic Medicine, University of Sheffield; ⁴ Royal Hallamshire Hospital, Sheffield, United Kingdom; ⁵ Christchurch Hospital, Christchurch, New Zealand; ⁶ Auckland Cancer Society Research Centre, Faculty of Medical and Health Sciences, University of Auckland, Auckland, New Zealand; and ⁷ Children's Medical Research Institute, Sydney, New South Wales, Australia

Requests for reprints: Janice A. Royds, Department of Pathology, Dunedin School of Medicine, University of Otago, P.O. Box 913, Dunedin, New Zealand. Phone: 64-3-4797471; Fax: 64-3-4797136; E-mail: Janice.royds{at}stonebow.otago.ac.nz.

The molecular basis for alternative lengthening of telomeres (ALT), a prognostic marker for glioma patients, remains unknown. We examined TP53 status in relation to telomere maintenance mechanism (TMM) in 108 patients with glioblastoma multiforme and two patients with anaplastic astrocytoma from New Zealand and United Kingdom. Tumor samples were analyzed with respect to telomerase activity, telomere length, and ALT-associated promyelocytic leukemia nuclear bodies to determine their TMM. TP53 mutation was analyzed by direct sequencing of coding exons 2 to 11. We found an association between TP53 mutation and ALT mechanism and between wild-type TP53 and telomerase and absence of a known TMM (P < 0.0001). We suggest that TP53 deficiency plays a permissive role in the activation of ALT. (Cancer Res 2006; 66(13): 6473-6)

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