By data from England, the overall 5-year survival rate of<unk>  is 67%. Between 20% and 50% of high-risk cases do not respond adequately to induction high-dose chemotherapy and are progressive or refractory. Relapse after completion of frontline therapy is also common. Further treatment is available in phase I and phase II clinical trials that test new agents and combinations of agents against<unk> , but the outcome remains very poor for relapsed high-risk disease. Most long-term survivors alive today had low or intermediate risk disease and milder courses of treatment compared to high-risk disease. The majority of survivors have long-term effects from the treatment. Survivors of intermediate and high-risk treatment often experience hearing loss, growth reduction, thyroid function disorders, learning difficulties, and greater risk of secondary cancers affect survivors of high-risk disease. An estimated two of three survivors of childhood cancer will ultimately develop at least one chronic and sometimes life-threatening health problem within 20 to 30 years after the cancer diagnosis. Cytogenetic profiles Based on a series of 493<unk>  samples, it has been reported that overall genomic pattern, as tested by array-based karyotyping, is a predictor of outcome in<unk> : *Tumors presenting exclusively with whole chromosome copy number changes were associated with excellent survival. *Tumors presenting with any kind of segmental chromosome copy number changes were associated with a high risk of relapse. *Within tumors showing segmental alterations, additional independent predictors of decreased overall survival were N-myc amplification, 1p and 11q deletions, and 1q gain. Earlier publications categorized<unk> s into three major subtypes based on cytogenetic profiles: *Subtype 1: favorable<unk>  with near triploidy and a predominance of numerical gains and losses, mostly representing non-metastatic<unk>  stages 1, 2 and 4S. *Subtypes 2A and 2B: found in unfavorable widespread<unk> , stages 3 and 4, with 11q loss and 17q gain without N-myc amplification (subtype 2A) or with N-myc amplification often together with 1p deletions and 17q gain (subtype 2B). Virtual karyotyping can be performed on fresh or paraffin-embedded tumors to assess copy number at these loci. SNP array virtual karyotyping is preferred for tumor samples, including<unk> s, because they can detect copy neutral loss of heterozygosity (acquired uniparental disomy). Copy neutral LOH can be biologically equivalent to a deletion and has been detected at key loci in<unk> . ArrayCGH, FISH, or conventional cytogenetics cannot detect copy neutral LOH.
Neuroblastoma
Ewing's sarcoma
Central neurocytoma
Astroblastoma
Neurothekeoma
Germinoma
Sialoblastoma
Neuroma