Endemic Burkitt lymphoma occurs at a high incidence in areas with high levels of infection with the parasite Plasmodium falciparum, which causes malaria. However, whether Plasmodium influences lymphomagenesis is not clear. Robbiani et al. used Plasmodium chabaudi infection to induce chronic malaria in mice and found that P. chabaudi induces expansion of germinal centres (GCs). GC B cells in P. chabaudi-infected mice expressed the mutator enzyme activation-induced cytidine deaminase (AID) and had increased DNA damage and chromosomal translocations. Mice lacking p53 in B cells develop lymphoma; P. chabaudi infection did not change the incidence of lymphoma in these mice but it favoured the development of AID-dependent mature B cell lymphomas that carried chromosomal translocations.
References
Robbiani, D. F. et al. Plasmodium infection promotes genomic instability and AID-dependent B cell lymphoma. Cell 162, 727–737 (2015)
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Seton-Rogers, S. A malaria mechanism. Nat Rev Cancer 15, 574 (2015). https://doi.org/10.1038/nrc4020
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DOI: https://doi.org/10.1038/nrc4020