Abstract:
:Although Epstein-Barr virus (EBV) infection is widely distributed, certain EBV-driven malignancies are geographically restricted. EBV-associated Burkitt's lymphoma (eBL) is endemic in children living in sub-Saharan Africa. This population is heavily exposed to food contaminated with the mycotoxin aflatoxin B1 (AFB1). Here, we show that exposure to AFB1 in in vitro and in vivo models induces activation of the EBV lytic cycle and increases EBV load, two events that are associated with an increased risk of eBL in vivo. AFB1 treatment leads to the alteration of cellular gene expression, with consequent activations of signaling pathways, e.g. PI3K, that in turn mediate reactivation of the EBV life cycle. Finally, we show that AFB1 triggers EBV-driven cellular transformation both in primary human B cells and in a humanized animal model. In summary, our data provide evidence for a role of AFB1 as a cofactor in EBV-mediated carcinogenesis.
journal_name
Carcinogenesisjournal_title
Carcinogenesisauthors
Accardi R,Gruffat H,Sirand C,Fusil F,Gheit T,Hernandez-Vargas H,Le Calvez-Kelm F,Traverse-Glehen A,Cosset FL,Manet E,Wild CP,Tommasino Mdoi
10.1093/carcin/bgv142subject
Has Abstractpub_date
2015-11-01 00:00:00pages
1440-51issue
11eissn
0143-3334issn
1460-2180pii
bgv142journal_volume
36pub_type
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