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Int J Cancer. 2008 Jul 15;123(2):436-443. doi: 10.1002/ijc.23486.

Fetal growth and the risk of childhood CNS tumors and lymphomas in Western Australia.

Author information

1
Telethon Institute for Child Health Research, Centre for Child Health Research,The University of Western Australia, Perth, Western Australia.
2
Princess Margaret Hospital and King Edward Memorial Hospital for Women, Subiaco, Perth, Western Australia.
3
Schools of Paediatrics and Child Health, and Women and Infants Health, University of Western Australia.

Abstract

The etiology of childhood cancers is largely unknown, although the early age at diagnosis has led to particular interest in in utero and perinatal factors. Birth weight is the most frequently studied perinatal factor in relation to risk of childhood cancers, and results have been inconsistent. We investigated whether the risk of CNS tumors and lymphomas in children was associated with three measures of the appropriateness of intra-uterine growth: proportion of optimal birth weight (POBW), birth length (POBL) and weight for length (POWFL). A cohort of 576,633 infants born in Western Australia in 1980-2004 were followed from birth to diagnosis of a CNS tumor (n = 183) or lymphoma (n = 84) before age 15, death, or December 31, 2005, and analyzed with Cox regression. Overall, there was little evidence of any association between fetal growth and risk of CNS tumors, although risk of ependymoma/choroid plexus tumors was positively associated with POBL and negatively associated with POWFL. The risk of Hodgkin and Burkitt lymphoma increased with increasing fetal growth among boys only, whereas the increased risk observed with non-Hodgkin lymphoma was only in girls. These associations between fetal growth and disease risk were also observed among children not classified as high birth weight, suggesting that accelerated growth is more important than birth weight per se. Results were similar when cases were compared with their unaffected siblings, suggesting that the increased growth associated with cancer risk was not general to the family. The associations we observed are consistent with causal pathways involving fetal growth factors.

PMID:
18412242
DOI:
10.1002/ijc.23486
[Indexed for MEDLINE]
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