Neuroblastoma is a form of embryonal neuroendocrine tumor that arises from neural crest progenitor cells, which can differentiate into multiple cell types. It is caused by genetic abnormalities such as MYCN oncogene amplification and 11q deletion, both of which can deregulate neuroblastoma suppressor genes located on chromosome 11q. MiRNAs are noncoding RNAs with an average length of 22 nucleotides. By binding to the 3′ untranslated regions of target messenger RNA, the RISC represses protein synthesis. The aim of this experimental project was to determine the effects of MYCN amplification or 11q deletion on the expression level of the miRNA, hsa-miR-34b-3p in neuroblastoma. The total RNA was extracted from the neuroblastoma cell lines, NB69 without MYCN amplification and 11q deletion, Kelly with 11q deletion and SK-NBE(2) with MYCN amplification. cDNAs were generated from the miRNA, hsa-miR-34b-3p located on chromosome 11q and the reference gene, RNU6B. The cDNAs were amplified and quantified by qPCR. The qPCR data were analysed using the comparative Ct method, Kruskal-Wallis test with multiple comparisons to determine whether or not hsa-miR-34b-3p was significantly differentially expressed in Kelly and SK-N-BE(2) compared to NB69. The results showed that hsa-miR-34b-3pwas significantly downregulated in the cell lines, Kelly and SK-N-BE(2) compared to NB69. In conclusion, the findings of this study showed that hsa-miR-34b-3p is downregulated in Kelly and SK-N-BE(2) compared to NB69, and call for further research to investigate its clinical potential in the therapy of neuroblastoma.