The DOI matches its Crossref record; 172 of the 172 references it cites were found in a registry or an index.
A causal mechanism for childhood acute lymphoblastic leukaemia
Open accessAbstract
In this Review, I present evidence supporting a multifactorial causation of childhood acute lymphoblastic leukaemia (ALL), a major subtype of paediatric cancer. ALL evolves in two discrete steps. First, in utero initiation by fusion gene formation or hyperdiploidy generates a covert, pre-leukaemic clone. Second, in a small fraction of these cases, the postnatal acquisition of secondary genetic changes (primarily V(D)J recombination-activating protein (RAG) and activation-induced cytidine deaminase (AID)-driven copy number alterations in the case of ETS translocation variant 6 (ETV6)–runt-related transcription factor 1 (RUNX1)+ ALL) drives conversion to overt leukaemia. Epidemiological and modelling studies endorse a dual role for common infections. Microbial exposures earlier in life are protective but, in their absence, later infections trigger the critical secondary mutations. Risk is further modified by inherited genetics, chance and, probably, diet. Childhood ALL can be viewed as a paradoxical consequence of progress in modern societies, where behavioural changes have restrained early microbial exposure. This engenders an evolutionary mismatch between historical adaptations of the immune system and contemporary lifestyles. Childhood ALL may be a preventable cancer. In this Review, Greaves describes the evidence supporting the model that infections early in life reduce the risk of childhood common B cell precursor acute lymphoblastic leukaemia (BCP-ALL) development. Given this evidence, paediatric BCP-ALL may be a preventable cancer.
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Metadata
- Authors
- Greaves, M.
- Venue
- Nature Reviews Cancer
- Published
- 2018-05-21
- Volume
- 18
- Issue
- 8
- Pages
- 471-484
- ISSN
- 1474-175X (ISSN-L)
- 1474-1768
- OpenAlex
- W2804265396
- Cited by
- 558
- References
- 172
- FWCI
- 12.57
- Type
- journal article
- Language
- en
- Open access
- bronze
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