In this article, the epidemiology and aetiology of childhood cancer are reviewed. The aetiology of childhood cancer is not clear. Both genetic predisposition and environmental agents are likely to be involved. There is a vast amount of literature on the subject, and PubMed (www.ncbi.nlm.nih.gov/PubMed) has been utilised to find key references. This review also synthesises and updates findings from articles that have been discussed in previously published reviews.1–4
Studies of descriptive epidemiology are important for providing clues to aetiology. The main findings are summarised in Table 1.
Childhood leukaemia comprises three main sub-types: acute lymphoblastic leukaemia (ALL), acute non-lymphocytic leukaemia (ANLL) and chronic myeloid leukaemia (CML). Childhood leukaemia is dominated by ALL, whereas CML is rare in this age group.
There is a marked variation in the incidence of ALL between countries, with a general trend for the incidence to be lower in less affluent populations and higher in more affluent populations. An incidence peak of ALL is found in more affluent populations in those one to four years of age and mainly comprises cases of the precursor B-cell subtype.1–4 This pattern is consistent with three recent aetiological hypotheses related to infections.5–8 Earlier exposure to infections may provide early priming of the immune system and consequently greater protection. In more affluent populations there is a general tendency for delay in exposure to infections compared with less affluent populations. The geographical patterning of ANLL is less clear.1–4
In contrast to leukaemia, the incidence of Hodgkin’s lymphoma (HL) is higher in less affluent populations. Burkitt lymphoma (BL) is associated with the Epstein-Barr virus (EBV) and is prevalent in certain malaria-endemic parts of sub-Saharan Africa and Papua New Guinea. Other types of non-Hodgkin’s lymphoma (NHL) do not show clear geographical patterns.1,3,4
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