Recent research published in The Journal of Immunology has revealed important insights into how Plasmodium falciparum infection, which causes malaria, contributes to the development of Burkitt lymphoma (BL). This finding helps explain why BL is the most prevalent childhood cancer in equatorial Africa and New Guinea.
Long-Standing Connection Finally Explained
Scientists have recognized an association between BL and P. falciparum malaria since the late 1950s, but until now, researchers couldn't explain the biological mechanism behind this connection.
"The discovery that malaria directly increases childhood cancer risk suggests that efforts to reduce P. falciparum malaria in Africa could simultaneously decrease Burkitt lymphoma cases," explained the study's lead researcher, Dr. Rosemary Rochford from the University of Colorado Anschutz School of Medicine, where she serves as Distinguished Professor of Immunology and Microbiology.
Cancer of the Immune System
Burkitt lymphoma affects B cells, which are critical immune system components responsible for antibody production. While BL remains rare worldwide, its frequency is ten times higher in regions where P. falciparum malaria is endemic. Notably, although humans can contract malaria from five different Plasmodium species, only P. falciparum shows this strong association with Burkitt lymphoma.
Enzyme Activity Reveals the Link
The researchers discovered significantly increased levels of an enzyme called activation-induced cytidine deaminase (AID) in B cells of children infected with P. falciparum malaria. This finding is particularly significant because AID plays a crucial role in BL development.
One characteristic feature of Burkitt lymphoma is the translocation of the MYC gene—a genetic abnormality where DNA breaks away from one chromosome and attaches to another. Since AID is essential for this MYC translocation process, its elevated presence in malaria patients provides strong evidence of P. falciparum's role in causing BL.
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Study Methodology and Findings
The research team compared blood samples from children with uncomplicated malaria (characterized by non-specific symptoms like fever, chills, headache, and nausea without severe organ dysfunction) to samples from children without malaria. Their analysis revealed that AID was not only significantly elevated in the B cells of children with uncomplicated malaria but was also fully functional—further supporting P. falciparum's role in BL development.
Future Research Directions
"We hope this study contributes to the growing evidence highlighting AID's critical role in Burkitt lymphoma etiology and potentially in other non-Hodgkin's lymphomas," noted Dr. Rochford.
Her team continues to investigate other effects of P. falciparum on children's immune function and how these changes create conditions favorable for cancer development.
Access to Research
The complete research article can be found in The Journal of Immunology or through AAI News. Those interested in obtaining a PDF copy of the research can contact the American Association of Immunologists.
About The American Association of Immunologists
The American Association of Immunologists (AAI) represents one of the world's largest communities of immunologists and scientists in related fields. The organization aims to enhance global health and well-being by advancing immunology and increasing public understanding of the immune system. AAI members have contributed to many significant biomedical breakthroughs of the past century, including cancer immunotherapies, antibody treatments, transplantation technologies, and vaccine development. The association supports immunology researchers through knowledge dissemination, community building, advocacy, and public education.
About The Journal of Immunology
The Journal of Immunology publishes peer-reviewed research describing new findings across all experimental immunology areas, encompassing both basic and clinical research. The journal is owned by the American Association of Immunologists and published in partnership with Oxford University Press.
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