Introduction Although rare, cancer is a leading cause of disease mortality in children after accidents, homicides, and suicides (Ries et al., 1999). The biology of cancer in children is markedly different to cancer in adults. This is highlighted by the disparate incidence and etiology of common cancers found between children and adults (AIHW and AACR, 2004). In children, leukemia and brain tumors predominate in newly diagnosed cases, while breast, colorectal, melanoma, and lung cancer are common cancers in adults. While there seems to be a genetic basis for adult cancers, where familial cases of breast (reviewed in Narod and Foulkes, 2004) and colorectal (reviewed in Jasperson et al., 2010) cancer have identified mutations of candidate risk genes, the same can not be said for childhood cancer. The precise causes of childhood cancer still remain unknown. With the scarce number of cases of familial or inherited cancers in children, it would seem that genetics plays a minor role in childhood cancer. Tumours acquire somatic mutation during their progression to cancer and it has long been hypothesized that selected environmental exposures can accelerate mutation rate in tumours that have given rise to their presentation as cancer in children (Knudson, 1976). There is a proposed list of high-risk exposures including radiation, infection, and pesticides associated with childhood cancer (reviewed in Anderson, 2006); however, the small study numbers used to identify these factors have led to small effect sizes and have been difficult to reproduce. Large, multi-center prospective cohort studies have begun to address this issue (Brown et al., 2007).
|Title of host publication||Epigenomics: From Chromatin Biology to Therapeutics|
|Publisher||Cambridge University Press|
|Number of pages||9|
|Publication status||Published - 1 Jan 2012|