DOCK8是神经母细胞瘤患者复发病例中特异且经常发生的突变基因，从R2数据库大量患者的mRNA数据分析得知DOCK8与MYCN基因存在显著的负相关性。约25%的该肿瘤患儿MYCN基因都有扩增，从诊断到复发的各个时期所取的神经母细胞瘤组织，均可检测到MYCN有一致的高表达，说明MYCN的高表达是高危性神经母细胞瘤的一种稳定的、固有的特性。且与正常肾上腺组织中DOCK8的表达量相比，在该肿瘤的每个时期DOCK8都呈显著性低表达，值得注意的是：与DOCK8低表达的患者相比，DOCK8高表达的患者生存期明显延长。多项数据分析强烈表明DOCK8在该肿瘤中可能起到了抑癌功能。本研究的目的是检测DOCK8是否能抑制MYCN诱导的神经母细胞瘤的肿瘤生成，并进一步探索DOCK8在该肿瘤形成过程中的细胞生命活动以及肿瘤形成与维持的分子机制，为神经母细胞瘤DOCK8分子及相应信号通路靶向治疗提供新的理论基础。

DOCK8 is one of the recurrent mutations in primary and relapsed neuroblastoma. In addition, there is a significant negative correlation between DOCK8 and MYCN in the microarray data analysis of a large number of neuroblastoma patients from the R2: microarray analysis and visualization platform (http://r2.amc.nl). MYCN amplification is present in about 25% of neuroblastomas and is associated with advanced stage disease and a poor prognosis. Consistent high expression of MYCN is detected in the different stages of diagnosis and recurrence, which means high MYCN expression is the steady and inherent characteristics of high-risk neuroblastoma. Compared with the expression of DOCK8 in the normal adrenal gland, there is a significant lower expression of DOCK8 at every stage of neuroblastoma. It is worth noting that comparing with patients with low expression of DOCK8, the survival period of the patients with high expression of DOCK8 was significantly prolonged. These emerging data analysis strongly suggest that DOCK8 may act as a tumor suppressor gene in human neuroblastoma. The purpose of this project is to detect whether DOCK8 could inhibit the tumorigenesis in MYCN induced neuroblastoma. And further to explore the molecular mechanism of DOCK8 in tumorigenesis and maintenance, as well as clarify cell activity in the process of tumor formation, which provides a novel theoretical basis for targeting DOCK8 and corresponding signaling pathways in the molecule-targeted treatment of neuroblastoma.