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SNP array analysis reveals novel genomic abnormalities including copy neutral loss of heterozygosity in anaplastic oligodendrogliomas

Ahmed Idbaih 1, 2 François Ducray 3 Caroline Dehais 4 Célia Courdy 5 Catherine Carpentier 1 Simon de Bernard 6 Emmanuelle Uro-Coste 7 Karima Mokhtari 8 Anne Jouvet 5 Jérôme Honnorat 9 Olivier Chinot 5 Carole Ramirez 10 Patrick Beauchesne 11 Alexandra Benouaich-Amiel 12 Joël Godard 13 Sandrine Eimer 14 Fabrice Parker 15 Emmanuelle Lechapt-Zalcman 16 Philippe Colin 17 Delphine Loussouarn 18 Thierry Faillot 19 Phong Dam-Hieu 20 Selma Elouadhani-Hamdi 21 Luc Bauchet 22 Olivier Langlois 23 Caroline Le Guerinel 24 Denys Fontaine 25 Elodie Vauleon 26 Philippe Menei 27, 28 Marie Janette Motsuo Fotso 29 Christine Desenclos 30 Pierre Verrelle 31 François Ghiringhelli 32, 33 Georges Noel 34 François Labrousse 35, 36, 37 Antoine Carpentier 38 Frédéric Dhermain 39, 40 Jean-Yves Delattre 1, 2 Dominique Figarella-Branger 5, *
* Auteur correspondant
Abstract : Anaplastic oligodendrogliomas (AOD) are rare glial tumors in adults with relative homogeneous clinical, radiological and histological features at the time of diagnosis but dramatically various clinical courses. Studies have identified several molecular abnormalities with clinical or biological relevance to AOD (e.g. t(1;19)(q10;p10), IDH1, IDH2, CIC and FUBP1 mutations).To better characterize the clinical and biological behavior of this tumor type, the creation of a national multicentric network, named "Prise en charge des OLigodendrogliomes Anaplasiques (POLA)," has been supported by the Institut National du Cancer (InCA). Newly diagnosed and centrally validated AOD patients and their related biological material (tumor and blood samples) were prospectively included in the POLA clinical database and tissue bank, respectively.At the molecular level, we have conducted a high-resolution single nucleotide polymorphism array analysis, which included 83 patients. Despite a careful central pathological review, AOD have been found to exhibit heterogeneous genomic features. A total of 82% of the tumors exhibited a 1p/19q-co-deletion, while 18% harbor a distinct chromosome pattern. Novel focal abnormalities, including homozygously deleted, amplified and disrupted regions, have been identified. Recurring copy neutral losses of heterozygosity (CNLOH) inducing the modulation of gene expression have also been discovered. CNLOH in the CDKN2A locus was associated with protein silencing in 1/3 of the cases. In addition, FUBP1 homozygous deletion was detected in one case suggesting a putative tumor suppressor role of FUBP1 in AOD.Our study showed that the genomic and pathological analyses of AOD are synergistic in detecting relevant clinical and biological subgroups of AOD.
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Ahmed Idbaih, François Ducray, Caroline Dehais, Célia Courdy, Catherine Carpentier, et al.. SNP array analysis reveals novel genomic abnormalities including copy neutral loss of heterozygosity in anaplastic oligodendrogliomas. PLoS ONE, Public Library of Science, 2012, 7 (10), pp.e45950. ⟨10.1371/journal.pone.0045950⟩. ⟨hal-00911465⟩

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