Abstract:
:The prerequisite to prevent childhood B-cell acute lymphoblastic leukemia (B-ALL) is to decipher its etiology. The current model suggests that infection triggers B-ALL development through induction of activation-induced cytidine deaminase (AID; also known as AICDA) in precursor B-cells. This evidence has been largely acquired through the use of ex vivo functional studies. However, whether this mechanism governs native non-transplant B-ALL development is unknown. Here we show that, surprisingly, AID genetic deletion does not affect B-ALL development in Pax5-haploinsufficient mice prone to B-ALL upon natural infection exposure. We next test the effect of premature AID expression from earliest pro-B-cell stages in B-cell transformation. The generation of AID off-target mutagenic activity in precursor B-cells does not promote B-ALL. Likewise, known drivers of human B-ALL are not preferentially targeted by AID. Overall these results suggest that infections promote B-ALL through AID-independent mechanisms, providing evidence for a new model of childhood B-ALL development.
journal_name
Nat Communjournal_title
Nature communicationsauthors
Rodríguez-Hernández G,Opitz FV,Delgado P,Walter C,Álvarez-Prado ÁF,González-Herrero I,Auer F,Fischer U,Janssen S,Bartenhagen C,Raboso-Gallego J,Casado-García A,Orfao A,Blanco O,Alonso-López D,Rivas JL,Tena-Dávila SG,Müsdoi
10.1038/s41467-019-13570-ysubject
Has Abstractpub_date
2019-12-05 00:00:00pages
5563issue
1issn
2041-1723pii
10.1038/s41467-019-13570-yjournal_volume
10pub_type
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