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Review
. 2021 May;35(5):1258-1264.
doi: 10.1038/s41375-021-01211-7. Epub 2021 Apr 9.

Can we prevent childhood Leukaemia?

Mel Greaves  1 , Valeria Cazzaniga  2 , Anthony Ford  2
Affiliations
Review

Can we prevent childhood Leukaemia?

Mel Greaves et al. Leukemia. 2021 May.
No abstract available

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Conflict of interest statement

The authors declare no competing interests.

Figures

Fig. 1
Fig. 1. The two-hit model for B cell precursor ALL.
Initiating genetic lesions are primarily ETV6-RUNX1 or hyperdiploidy, probably occurring as developmental accidents. They arise in utero possibly in foetal liver early B lineage lymphopoiesis [78]. Secondary mutations are primarily RAG-mediated copy number alterations. ~1% figure: ALL is initiated in utero at a rate that exceeds by 100-fold, the incidence of disease indicating a low penetrance and a critical role for factors promoting chronic inflammation and the secondary mutations. Adapted from [7]. See text for references.
Fig. 2
Fig. 2. Environmental, life exposures that source and impact on the infant microbiome.
Of the five critical factors, three (✓ in figure) have been implicated as risk factors in B cell precursor ALL. Birth route—vaginal versus caesarean. Note: diet and antibiotics also impact on the composition of the microbiome but those two variables have not been systematically evaluated for impact on the risk of ALL.
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