Journal
CELL
Volume 162, Issue 4, Pages 727-737Publisher
CELL PRESS
DOI: 10.1016/j.cell.2015.07.019
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Funding
- Worldwide Cancer Research [11-0022]
- Fondazione Ettore e Valeria Rossi
- NIH [AI112602, AI037526, AI072529]
- NIH, the National Cancer Institute, the Center for Cancer Research
- Department of Defense grant (BCRP DOD Idea Expansion Award) [11557134]
- Worldwide Cancer Research [11-0022] Funding Source: researchfish
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Chronic infection with Plasmodium falciparum was epidemiologically associated with endemic Burkitt's lymphoma, a mature B cell cancer characterized by chromosome translocation between the c-myc oncogene and Igh, over 50 years ago. Whether infection promotes B cell lymphoma, and if so by which mechanism, remains unknown. To investigate the relationship between parasitic disease and lymphomagenesis, we used Plasmodium chabaudi (Pc) to produce chronic malaria infection in mice. Pc induces prolonged expansion of germinal centers (GCs), unique compartments in which B cells undergo rapid clonal expansion and express activation-induced cytidine deaminase (AID), a DNA mutator. GC B cells elicited during Pc infection suffer widespread DNA damage, leading to chromosome translocations. Although infection does not change the overall rate, it modifies lymphomagenesis to favor mature B cell lymphomas that are AID dependent and show chromosome translocations. Thus, malaria infection favors mature B cell cancers by eliciting protracted AID expression in GC B cells.
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