ABSTRACT
This chapter discusses mechanisms of carcinogenesis, incidence of childhood cancer, cancer treatment, neuroblastoma, nephroblastoma (wilms tumour), soft tissue sarcomas, bone tumours, retinoblastoma, gonadal and germ cell tumours, liver tumours, brain tumours, leukaemias, lymphoma, and childhood histiocytosis syndromes. It provides clinical manifestations, prognostic features, investigations, and management of the diseases. Cancer develops when there is genetic alteration of the normal cell regulatory system (growth and development) via mutation(s). Cancer-causing genes fall into three types. Tumour suppressor genes, Oncogenes and DNA repair genes. Mutations activating the cancer genes can be germline, somatic or both. The environment can increase the frequency of genetic mutations. Two-hit theory of carcinogenesis is that a tumour will develop only when both copies of a gene are damaged. In many inherited cancers, the first allele is a germline mutation and the second a somatic mutation. This would explain why not all children who inherit the retinoblastoma mutation develop the tumour, and that they develop it at different ages.
