{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Rodriguez-Hernandez G"],"funding":["European Research Council"],"pagination":["5563"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6895129"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["10(1)"],"pubmed_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 p"],"journal":["Nature communications"],"pubmed_title":["Infectious stimuli promote malignant B-cell acute lymphoblastic leukemia in the absence of AID."],"pmcid":["PMC6895129"],"funding_grant_id":["207844"],"pubmed_authors":["Alonso-Lopez D","Tena-Davila SG","Ramiro AR","Raboso-Gallego J","Blanco O","Rodriguez-Hernandez G","Orfao A","Borkhardt A","Criado FJG","Sanchez-Garcia I","Dugas M","Cenador MBG","Vicente-Duenas C","Opitz FV","Fischer U","Alvarez-Prado AF","Walter C","Muschen M","Gonzalez-Herrero I","Rivas JL","Casado-Garcia A","Auer F","Delgado P","Bartenhagen C","Hauer J","Janssen S"],"additional_accession":[]},"is_claimable":false,"name":"Infectious stimuli promote malignant B-cell acute lymphoblastic leukemia in the absence of AID.","description":"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 p","dates":{"release":"2019-01-01T00:00:00Z","publication":"2019 Dec","modification":"2026-05-05T01:01:11.116Z","creation":"2020-05-21T21:21:09Z"},"accession":"S-EPMC6895129","cross_references":{"pubmed":["31804490"],"doi":["10.1038/s41467-019-13570-y"]}}