IJE Advance Access published online on January 25, 2007
International Journal of Epidemiology, doi:10.1093/ije/dyl299
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Published by Oxford University Press on behalf of the International Epidemiological Association © The Author 2007; all rights reserved.
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Cohort Profile: The International Childhood Cancer Cohort Consortium (I4C)
1 National Center for Environmental Assessment, Office of Research and Development, U.S. Environmental Protection Agency, Washington, DC, USA.
2 Murdoch Childrens Research Institute, Melbourne, Australia.
3 National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Rockville, MD, USA.
4 National Institute of Child Health and Human Development, National Institutes of Health, Department of Health and Human Services, Rockville, MD, USA.
5 National Center for Maternal and Infant Health, Peking University Health Science Center, Beijing, China.
6 Department of Epidemiology, University of California, Los Angeles, CA, USA.
* Corresponding author. U.S. Environmental Protection Agency, National Center for Environmental Assessment, 1200 Pennsylvania Avenue, NW, 8623D, Washington, DC, 20460 USA. E-mail: brown.rebecca@epa.gov
Accepted 7 December 2006
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Globally, a number of large infant/child prospective studies have been launched to examine environmental and genetic determinants of common diseases of children, such as asthma, developmental delay and behaviour abnormalities, as well as the consequences of early exposure for adult diseases. While several of these studies are relatively very largeover 100 000 subjectsand are adequately powered to examine their principal outcomes of interest, none of the individual studies are of sufficient size to examine the relationship between exposures they are measuring and rare diseases such as childhood cancer. To date, the few established risk factors for specific forms of childhood cancer have largely been identified in case-control studies. Yet, despite many such investigations evaluating postulated risk factors for paediatric malignancies during the past five decades, few consistently established aetiologic factors are known. Recent review papers14 have summarized many promising hypotheses, including pre-natal and post-natal exposure to pesticides, maternal and early
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Chromosomal Rearrangements
Folic Acid Supplementation and Genetic Polymorphisms
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