Objective: To detect N-MYC gene copy number alterations, and to analyze their related clinicopathological implications in pediatric neuroblastic tumors (NTs). Methods: A total of 483 NT samples were obtained, including 388 neuroblastomas (NBs), 89 ganglioneuroblastomas (GNBs) and 6 ganglioneuromas (GNs). Fluorescence in situ hybridization (FISH) was used to detect numerical aberrations of N-MYC. Statistical analysis was used to study its association with clinicopathological features, as well as with the survival rate of patients. Results: Of 483 NT cases, N-MYC amplification rate was 12.4%. Gene amplification of N-MYC were found only in NB, but not in any GNB or GN case (P<0.05). N-MYC gene amplification was more likely to occur in poorly differentiated neuroblastoma(P=0.01), the rate of which was inversely related to tumor differentiation. The N-MYC amplification rate in male patients was higher than that in female patients (P=0.05). There was a trend that the amplification rate of N-MYC gene was lower in patients ≤18 months as compared to patients >18 months, but difference was not significantly (P=0.092). The univariate survival analysis showed that the survival rate of patients with N-MYC gene amplification was significantly lower than those with N-MYC gain or normal gene status. Conclusion: N-MYC gene amplification is tightly correlated with tumor type, differentiation, gender, age and survival. Detection of abnormal N-MYC copy number would be helpful for the diagnosis and prognosis of neuroblastic tumors.