“…Neuroblastoma models in which MYCN is overexpressed in the neural crest lead to neuroblastoma tumor development, that is accelerated by cooperation with other oncogenes and tumor suppressor genes, such as ALK, NF1, TP53, LIN28B and LMO1, driving increased penetrance and earlier onset of neuroblastoma (63)(64)(65)(66)(67)(68). Other factors, which also contribute to neuroblastoma tumorigenesis, are loss of heterozygosity (LOH) for chromosome 14 (14q), loss of NF1 and CDKN2A, amplification of DDX1 and MDM2, aberrant expression of neurotrophin receptors, ganglioside GD2, polycomb complex protein Bmi-1, micro RNAs (miR-10b, miR-29a/b, miR-335), as well as mutations in PHOX2B, ATRX, CHEK2 and BARD1 (53,(69)(70)(71)(72)(73)(74)(75)(76)(77). In addition to protein coding genes, long noncoding RNAs, such as neuroblastoma associated transcript-1 (NBAT-1) and Cancer Susceptibility 15 (CASC15), regulate neuroblastoma tumorigenesis via cell proliferation and neuronal differentiation (78,79).…”