Abstract
Neuroblastoma is a solid malignancy observed in pediatric patients developing when neuroblasts are unable to mature, leading to unregulated proliferation and tumor formation. Neuroblastoma is heterogeneous and aggressive in nature, leading to high treatment failure, morbidity, and mortality rates. Lewis family glycans, as part of the Core 2 O-glycans, play a key role in neuroblastoma malignant cell behavior in MYCN-amplified cell lines. Current treatment approaches for neuroblastoma include chemotherapy, surgery, and radiation. These approaches are faced with physiological and cellular barriers, including the less understood role of glycosylation in development and treatment. Studies have confirmed that the inhibition of mucin glycosylation has improved effectiveness of cytotoxic drug agents employed against solid malignancies such as with pancreatic cancer, yet little research is available regarding the influence of glycosylated proteins for other diseases. This article explores genetic defects associated with neuroblastoma such MYCN gene amplification at the time of diagnosis, as well as clinical approaches and therapeutic challenges encountered during treatment. Additionally, the article reviews experimental and clinical evidence in support of the influence of glycosylation in neuroblastoma development, and possible unfavorable impact of glycosylation on drug therapy.