Association of Mutant TP53 with Alternative Lengthening of Telomeres and Favorable Prognosis in Glioma
2006; American Association for Cancer Research; Volume: 66; Issue: 13 Linguagem: Inglês
10.1158/0008-5472.can-06-0910
ISSN1538-7445
AutoresYu-Jen Chen, Vicky Hakin-Smith, Mario Teo, George Xinarianos, David Jellinek, Thomas Carroll, David McDowell, Martin R. MacFarlane, Ronald Boet, Bruce C. Baguley, Antony W. Braithwaite, Roger R. Reddel, Janice A. Royds,
Tópico(s)Cancer-related Molecular Pathways
ResumoAbstract 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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