The cause of<unk>  is not well understood. The great majority of cases are sporadic and nonfamilial. About 1–2% of cases run in families and have been linked to specific gene mutations. Familial<unk>  in some cases is caused by rare germline mutations in the anaplastic lymphoma kinase (ALK) gene. Germline mutations in the PHOX2B or KIF1B gene have been implicated in familial<unk> , as well.<unk>  is also a feature of neurofibromatosis type 1 and the Beckwith-Wiedemann syndrome. MYCN oncogene amplification within the tumor is a common finding in<unk> . The degree of amplification shows a bimodal distribution: either 3- to 10-fold, or 100- to 300-fold. The presence of this mutation is highly correlated to advanced stages of disease. Duplicated segments of the LMO1 gene within<unk>  tumor cells have been shown to increase the risk of developing an aggressive form of the cancer.<unk>  has been linked to copy-number variation within the<unk> PF10 gene, which results in the 1q21.1 deletion syndrome or 1q21.1 duplication syndrome. Several risk factors have been proposed and are the subject of ongoing research. Due to characteristic early onset, many studies have focused on parental factors around conception and during gestation. Factors investigated have included occupation (i.e. exposure to chemicals in specific industries), smoking, alcohol consumption, use of medicinal drugs during pregnancy, and birth factors; however, results have been inconclusive. Other studies have examined possible links with atopy and exposure to infection early in life, use of hormones and fertility drugs, and maternal use of hair dye.
Neuroblastoma
Ewing's sarcoma
Central neurocytoma
Astroblastoma
Neurothekeoma
Germinoma
Sialoblastoma
Neuroma