Neuroblastoma is the most common extra-cranial solid tumour in infants and children, arising from sympathoadrenal progenitor cells. Recently, DLG2 under-expression was found in 11q-deleted and MYCN-amplified neuroblastoma, both aggressive onset of tumours. MYCN and DLG are well-known for their role as an oncogene and tumour suppressor, respectively. The aim of this project is to analyse the effect of Dlg silencing and dMyc over-expression on gene expression. Drosophila was used as a neuroblastoma model. The UAS-GAL4 system was used to induce Dlg silencing and dMyc over-expression in Drosophila nerve cells and neuroblasts. Adult fly heads were dissected. RNA was purified. RT-qPCR was performed to analyse expression of several genes. Results showed that both induced mutations affected similarly expression of analysed genes, suggesting a correlation between Dlg and dMyc proteins. CASK was down-regulated (log2FC = -1.65, p = 0.0088) (log2FC = -0.98, p = 0.0214) and metro was up-regulated (log2FC = 0.90, p = 0.0050) (log2FC = 1.88, p = 0.0027). All analysed cyclins were over-expressed. XRCC1 (log2FC = 0.71, p = 0.0124) and mre11 (log2FC = 1.94, p = 0.0123) were up-regulated in neuroblasts. We conclude that Dlg silencing and dMyc over-expression cause a dysregulation of genes involved in apico-basal cell polarity, cell cycle and DNA repair mechanisms: altered cyclins indicate an uncontrolled progression through the cell cycle; low levels of metro suggest a role in a compensatory mechanism in cell polarity; and mre11 and XRCC1 up-regulation in neuroblasts reveal that alternative nonhomologous end-joining might be involved in aggressive neuroblastoma.