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Neurology 2003;60:1820-1822
© 2003 American Academy of Neurology
Brief Communications

Telomerase reactivation in malignant gliomas and loss of heterozygosity on 10p15.1

P. Leuraud, MSc, L. Aguirre-Cruz, MD, K. Hoang-Xuan, MD, E. Crinière, MSc, M-L. Tanguy, MD, J-L. Golmard, MD PhD, M. Kujas, MD, J-Y. Delattre, MD and M. Sanson, MD PhD

From the INSERM U495 (Drs. Aguirre-Cruz, Hoang-Xuan, Delattre, and Sanson, P. Leuraud and E. Crinière), Laboratoire de Biologie des Interactions Neurones-Glie, Fédération de Neurologie Mazarin (Drs. Hoang-Xuan, Delattre, and Sanson), Service de Biostatistique (Drs. Tanguy and Golmard), and Laboratoire d’Histologie-Embryologie-Cytogénétique (Dr. Kujas), Groupe hospitalier Pitié-Salpêtrière and Université Pierre et Marie Curie, Paris, France.

Address correspondence and reprint requests to Dr. Marc Sanson, Clinique Neurologique, Hôpital de la Salpêtrière, 47, Bd de l’Hôpital, 75634 Paris cedex 13, France; e-mail: m.sanson{at}psl.ap-hop-paris.fr

An inhibitor of telomerase activity maps to chromosome 10p15.1. A series of 51 high-grade gliomas was analyzed for loss of heterozygosity (LOH) on chromosome 10 and for telomerase activity. In univariate analysis, LOH10p (59%) and LOH10q (61%) were associated with telomerase activity (55%; p < 0.0001 and p = 0.0006). In multivariate analysis, only LOH10p remained statistically related to telomerase activity, suggesting that the telomerase repressor gene located on 10p15.1 is inactivated in high-grade gliomas.




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[Abstract] [Full Text] [PDF]


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