(In)flaming susceptibility

Alderton, Gemma K.

doi:10.1038/nrc.2015.14

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Published: 23 December 2015

Ageing

(In)flaming susceptibility

Gemma K. Alderton

Nature Reviews Cancer volume 16, page 5 (2016)Cite this article

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Cancer incidence increases with age, but the mechanisms underlying this effect remain unclear. Henry et al. showed that B cell progenitor cells had defective signalling and metabolism, as well as altered gene expression. These defects were recapitulated in B cell progenitors derived from young mice when they were transplanted into old mice. The reduced fitness that resulted from these changes was reversed by expression of oncogenes such as Myc, leading to leukaemogenesis. Ageing was associated with bone marrow inflammation, and when this was reduced through expression of α1-antitrypsin or interleukin-37 (IL-37), B cell progenitors were functional and resisted NRAS^G12V-mediated transformation. Thus, inflammation-exposed B cell progenitors are more liable to undergo transformation than those from young mice that are not situated in an inflammatory microenvironment.

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References

Henry, C. J. et al. Aging-associated inflammation promotes selection for adaptive oncogenic events in B cell progenitors. J. Clin. Invest. 125, 4666–4680 (2015)
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