Identification of MET genomic amplification, protein expression and alternative splice isoforms in neuroblastomas

摘要: Background Crizotinib, a dual anaplastic lymphoma kinase (ALK) and mesenchymal-epithelial transition (MET) tyrosine inhibitor, is currently being evaluated for the treatment of neuroblastoma. Its effects are thought to be mediated mainly via its activity against ALK. Although MET genomic/protein expression status might conceivably affect crizotinib efficacy, this issue has hitherto not received attention in neuroblastomas. Aims/Methods genomic protein was characterised by silver situ hybridisation immunohistochemistry (IHC) respectively, cohort 54 neuroblastoma samples. splice isoforms were 15 these samples quantitative PCR. Results One case (1/54; prevalence 1.85%) displayed amplification, while another strong membranous (IHC score 3+). Alternative exon 10-deleted 14-deleted identified. Conclusions amplification expression, although low prevalence, present This implications when employed as therapeutic agent Additionally, existence alternatively spliced may have clinical biological