American Journal of Epidemiology Advance Access originally published online on June 18, 2007
American Journal of Epidemiology 2007 166(3):365; doi:10.1093/aje/kwm159
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LETTERS TO THE EDITOR |
SEVERAL AUTHORS REPLY
From the Epidemiology and Genetics Unit, Department of Health Sciences, University of York, YO10 5DD York, United Kingdom
(e-mail: eve.roman{at}egu.york.ac.uk)
We thank Dorak et al. (1) for their interest in our recent findings from the United Kingdom Childhood Cancer Study (UKCCS) (www.ukccs.org) regarding the relation between infection in the first year of life and childhood leukemia (2).
Acute lymphoblastic leukemia (ALL) is a complex and heterogeneous disease, and as such there is unlikely to be a single causal mechanism (3). One of the most promising areas of research relates to the potential etiologic role of immune factors, and there has been much discussion about the timing and nature of infectious exposures in infancy—although hitherto the evidence base has been weak. Our analyses of contemporaneously compiled clinical data do not support the suggestion that a paucity of infectious exposure in the first year of life is associated with development of precursor B-cell ALL at 2–5 years of age—this is the hypothesis that was being tested. Rather, children who developed the common form of ALL were observed to have more infections, not fewer, in the first months of life. In addition, those with the most neonatal infections tended to be diagnosed earlier (see figure 1 in our paper (2, p. 502)).
Dorak et al. (1) point out that male sex confers an increased risk of ALL, and we agree that sex stratification should be more widely applied in analyses such as these. Indeed, within the UKCCS, findings often differ markedly for boys and girls, although the underlying reasons are likely to be more complex than simply sex alone (4). With respect to the infection data, however, among controls we found no difference in the frequency of clinically diagnosed infectious episodes between boys and girls (2).
The immunologic mechanism(s) underpinning the associations we observed remain to be clarified and were beyond the scope of the investigation. On the basis of the available data, it is not possible to determine whether our observations reflect the fact that children who develop ALL are more prone to infectious illness from an early age, or indeed whether infection(s) itself has a causal role. Furthermore, while infection is one possible marker of immune function, there are others. For example, within the UKCCS data there is also a strong inverse association between ALL and clinically diagnosed eczema (5). Accordingly, we are presently investigating the interplay between early infection, allergy, and subsequent leukemia development.
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ACKNOWLEDGMENTS |
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Conflict of interest: none declared.
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References |
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 TOP References |
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- Dorak MT, McNally RJQ, Parker L. Re: "Childhood acute lymphoblastic leukemia and infections in the first year of life: a report from the United Kingdom Childhood Cancer Study." (Letter). Am J Epidemiol (2007) 166:364–5.
[Free Full Text] - Roman E, Simpson J, Ansell P, et al. Childhood acute lymphoblastic leukemia and infections in the first year of life: a report from the United Kingdom Childhood Cancer Study. Am J Epidemiol (2006) 165:496–504.[CrossRef][ISI][Medline]
- Greaves M. Infection, immune responses and the aetiology of childhood leukaemia. Nat Rev Cancer (2006) 6:193–203.[CrossRef][ISI][Medline]
- Roman E, Simpson J, Ansell P, et al. Perinatal and reproductive factors: a report on haematological malignancies from the UKCCS. Eur J Cancer (2005) 41:749–59.[CrossRef][ISI][Medline]
- Hughes AM, Lightfoot T, Simpson J, et al. Allergy and risk of childhood leukaemia: results from the UKCCS. Int J Cancer (2007) Mar 27. [Epub ahead of print]. (DOI: 10.1002/ijc.22702).
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