| Literature DB >> 26276629 |
Davide F Robbiani1, Stephanie Deroubaix2, Niklas Feldhahn2, Thiago Y Oliveira2, Elsa Callen3, Qiao Wang2, Mila Jankovic2, Israel T Silva2, Philipp C Rommel2, David Bosque2, Tom Eisenreich2, André Nussenzweig3, Michel C Nussenzweig4.
Abstract
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. PAPERCLIP.Entities:
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Year: 2015 PMID： 26276629 PMCID： PMC4538708 DOI： 10.1016/j.cell.2015.07.019
Source DB: PubMed Journal: Cell ISSN： 0092-8674 Impact factor: 41.582