Bellini, AngelaBernard, VirginieAmbros, IngeAmbros, Peter F.de Preter, KatleenCombaret, ValérieBeiske, KlausJeison, MartaMarques, BarbaraMorini, MartinaMazzocco, KatiaDefferrari, RaffaellaBetts, DavidMartinsson, TommyMühlethaler-Mottet, AnnickNoguera, RosaFont de Mora, JaimeVicha, AlesLadenstein, RuthValteau-Couanet, DominiqueRossing, Caroline MariaBown, NickTweddle, DeborahAvigad, SmadarLapouble, EveChicard, MathieuLeprovost, NadaClement, NathalieBaulande, SylvainPierron, GaelleIrene, JimenezJaydutt, BhalshankarDelattre, OlivierMichon, JeanSchleiermacher, Gudrun2019-02-192019-02-192018-10-10http://hdl.handle.net/10400.18/5900Background: In neuroblastoma (NB), the ALK receptor tyrosine kinase can be constitutively activated either through genomic amplification or activating point mutations. We studied ALK genetic alterations in high-risk NB patients to determine their frequency and prognostic impact.engNeuroblastomaALKTumor GenomicsDoenças Genéticasconference object