Research Uncovers Link Between Malaria and Childhood Cancer

Recent findings published in The Journal of Immunology shed light on the connection between infections caused by Plasmodium falciparum, the parasite responsible for malaria, and the onset of Burkitt lymphoma (BL), which stands as the most prevalent childhood cancer in equatorial Africa and New Guinea. While the association between BL and P. falciparum has been noted since 1958, the precise biological mechanisms driving this relationship have remained largely unexplored.

Dr. Rosemary Rochford, a Distinguished Professor of Immunology and Microbiology at the University of Colorado Anschutz School of Medicine, emphasized the implications of this research, stating that understanding malaria's role in elevating childhood cancer risk could inform strategies aimed at reducing the incidence of P. falciparum in Africa, ultimately contributing to a decrease in Burkitt lymphoma cases.

Burkitt lymphoma primarily affects B cells, crucial components of the immune system responsible for antibody production. Although it is considered rare on a global scale, its occurrence is significantly higher--by a factor of ten--in regions where P. falciparum malaria is endemic. Among the five species of Plasmodium that can infect humans, only P. falciparum has been linked to Burkitt lymphoma.

This study identified a notable increase in the expression of an enzyme known as activation-induced cytidine deaminase (AID) in B cells from children suffering from malaria. This observation points to a direct involvement of P. falciparum in the pathogenesis of Burkitt lymphoma, given the established role of AID in the development of this cancer.

A defining feature of Burkitt lymphoma is the translocation of the MYC gene, a genetic alteration where DNA segments break from one chromosome and reattach to another. The presence of AID is crucial for this translocation process, indicating that elevated levels of this enzyme in malaria patients suggest a significant relationship between P. falciparum and Burkitt lymphoma.

The research involved analyzing blood samples from children diagnosed with uncomplicated malaria, comparing their AID levels to those from children without malaria. Uncomplicated malaria is characterized by general symptoms such as fever, chills, sweating, headache, nausea, and vomiting, without severe organ dysfunction.

The findings revealed that AID levels were markedly higher in B cells of children with uncomplicated malaria, and the elevated AID was fully functional. This further substantiates the hypothesis that P. falciparum plays a critical role in the development of Burkitt lymphoma.

Dr. Rochford expressed hope that this research will enhance the understanding of AID's vital role in the etiology of Burkitt lymphoma and potentially other forms of non-Hodgkin's lymphomas. Moving forward, her team aims to explore additional impacts of P. falciparum on immune function in children and how these effects may foster an environment conducive to cancer development.

For further reading, see the study by Bonface Ariera et al., titled Sustained activation induced cytidine deaminase (AID) expression in B cells following Plasmodium falciparum malaria infection in Kenyan children, published in The Journal of Immunology (2025).