• Marc Sanson, Pascal Leuraud, Lucinda Aguirre-Cruz, Jié He, Yannick Marie, Stéphanie Cartalat-Carel, Karima Mokhtari, Hugues Duffau, Jean-Yves Delattre, and Khê Hoang-Xuan.
• INSERM U495, Laboratoire de Biologie des Interactions Neurones-Glie, Groupe Hospitalier Pitié-Salpêtrière and Université Pierre et Marie Curie, Paris, France. m.sanson@psl.ap-hop-paris.fr
• J. Neurosurg. 2002 Dec 1; 97 (6): 1397-401.

ObjectChromosomal deletions of 10q and candidate genes such as PTEN and DMBT1 have been thoroughly investigated in glioblastomas but few data specifically address oligodendrogliomas.MethodsIn this study, 39 pure oligodendrogliomas were investigated for loss of heterozygosity (LOH) on 10q, PTEN mutations, and DMBT1 homozygous deletions. The LOH on 10q was found in 19 (48%) of 39 oligodendrogliomas and was closely related to anaplasia (p = 0.02), shorter time to progression (p = 0.0005), and poorer survival (p = 0.035). The DMBT1 homozygous deletions were found in 10 (26%) of 39 oligodendrogliomas but only one PTEN mutation was detected. The LOH on 10q is a strong predictor of survival and could be a valuable prognostic marker in oligodendrogliomas.ConclusionsFrequent inactivation of DMBT1 contrasting with rare mutations of PTEN may indicate that DMBT1 is preferentially involved in oligodendrogliomas. Nevertheless, the absence of a correlation with survival makes the role of DMBT1 in tumorigenesis still questionable and warrants further investigation.

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