Aetiology

• Childhood cancer generally represents aberrant growth and development rather than defective repair and renewal from which most adult tumours arise.

• Growths arising in infancy are mostly congenital and the genetic mutations concerned arise in utero. Causes of such mutations and those arising later in childhood largely unknown.

• Although isolated cases are attributable to high dose radiation (e.g. thyroid cancer in Chernobyl survivors), there is no convincing link to levels of background radiation or electromagnetic fields.

• Population mixing studies have suggested that patterns of exposure to infection may contribute to some cases of ALL in the peak years of incidence (2-6 years).

• Childhood cancer rarely familial, but study of retinoblastoma (rare tumour that is commonly familial) has led to better understanding of tumour suppressor genes; germline mutation in one allele of RB gene in affected families only gives rise to tumours in cells where there is an acquired mutation in the other, healthy, wild type allele (the 'two hit' hypothesis).

• Cancer arising in older children may still be due to intrauterine event as concordance studies in identical twins with ALL have shown identical genetic mutations in malignant cells some years after birth. This suggests twin—►twin transfer of potentially malignant clone through shared circulation.

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