Infectious stimuli promote malignant B-cell acute lymphoblastic leukemia in the absence of AID

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 evidenc...

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Autores: Rodríguez-Hernández, Guillermo, Opitz, Friederike V, Delgado, Pilar, Walter, Carolin, Alvarez-Prado, Angel Francisco, González-Herrero, Inés, Auer, Franziska, Fischer, Ute, Janssen, Stefan, Bartenhagen, Christoph, Raboso-Gallego, Javier, Casado-García, Ana, Orfao, Alberto, Blanco, Oscar, Alonso-López, Diego, Rivas, Javier De Las, Tena-Dávila, Sara González de, Müschen, Markus, Dugas, Martin, Criado, Francisco Javier García, Cenador, María Begoña García, Vicente-Dueñas, Carolina, Hauer, Julia, Ramiro, Almudena R, Sanchez-Garcia, Isidro, Borkhardt, Arndt
Tipo de recurso: artículo
Fecha de publicación:2019
País:España
Institución:Instituto de Salud Carlos III (ISCIII)
Repositorio:Repisalud
Idioma:inglés
OAI Identifier:oai:repisalud.isciii.es:20.500.12105/8953
Acceso en línea:http://hdl.handle.net/20.500.12105/8953
Access Level:acceso abierto
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spelling Infectious stimuli promote malignant B-cell acute lymphoblastic leukemia in the absence of AIDRodríguez-Hernández, GuillermoOpitz, Friederike VDelgado, PilarWalter, CarolinAlvarez-Prado, Angel FranciscoGonzález-Herrero, InésAuer, FranziskaFischer, UteJanssen, StefanBartenhagen, ChristophRaboso-Gallego, JavierCasado-García, AnaOrfao, AlbertoBlanco, OscarAlonso-López, DiegoRivas, Javier De LasTena-Dávila, Sara González deMüschen, MarkusDugas, MartinCriado, Francisco Javier GarcíaCenador, María Begoña GarcíaVicente-Dueñas, CarolinaHauer, JuliaRamiro, Almudena RSanchez-Garcia, IsidroBorkhardt, ArndtThe 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.SpringerUnión Europea. Fondo Europeo de Desarrollo Regional (FEDER/ERDF)Instituto de Salud Carlos IIIGerman Cancer Consortium (Alemania)Unión Europea. Comisión EuropeaUnión Europea. Comisión Europea. European Research Council (ERC)Ministerio de Ciencia, Innovación y Universidades (España)Fundación ProCNICDeutsche Forschungsgemeinschaft (Alemania)Junta de Castilla y León (España)20202020-01-2920192019-12-0520192019-12-05journal articlehttp://purl.org/coar/resource_type/c_6501VoRhttp://purl.org/coar/version/c_970fb48d4fbd8a85info:eu-repo/semantics/articleapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/vnd.openxmlformats-officedocument.spreadsheetml.sheetapplication/vnd.openxmlformats-officedocument.spreadsheetml.sheethttp://hdl.handle.net/20.500.12105/8953reponame:Repisaludinstname:Instituto de Salud Carlos III (ISCIII)InglésengES SEV-2015-0505 Not availableEuropean Commission http://dx.doi.org/10.13039/501100000780 Seventh Framework Programme 207844open accesshttp://purl.org/coar/access_right/c_abf2Atribución 4.0 Internacionalhttp://creativecommons.org/licenses/by/4.0/info:eu-repo/semantics/openAccessoai:repisalud.isciii.es:20.500.12105/89532026-06-12T12:43:37Z
dc.title.none.fl_str_mv Infectious stimuli promote malignant B-cell acute lymphoblastic leukemia in the absence of AID
title Infectious stimuli promote malignant B-cell acute lymphoblastic leukemia in the absence of AID
spellingShingle Infectious stimuli promote malignant B-cell acute lymphoblastic leukemia in the absence of AID
Rodríguez-Hernández, Guillermo
title_short Infectious stimuli promote malignant B-cell acute lymphoblastic leukemia in the absence of AID
title_full Infectious stimuli promote malignant B-cell acute lymphoblastic leukemia in the absence of AID
title_fullStr Infectious stimuli promote malignant B-cell acute lymphoblastic leukemia in the absence of AID
title_full_unstemmed Infectious stimuli promote malignant B-cell acute lymphoblastic leukemia in the absence of AID
title_sort Infectious stimuli promote malignant B-cell acute lymphoblastic leukemia in the absence of AID
dc.creator.none.fl_str_mv Rodríguez-Hernández, Guillermo
Opitz, Friederike V
Delgado, Pilar
Walter, Carolin
Alvarez-Prado, Angel Francisco
González-Herrero, Inés
Auer, Franziska
Fischer, Ute
Janssen, Stefan
Bartenhagen, Christoph
Raboso-Gallego, Javier
Casado-García, Ana
Orfao, Alberto
Blanco, Oscar
Alonso-López, Diego
Rivas, Javier De Las
Tena-Dávila, Sara González de
Müschen, Markus
Dugas, Martin
Criado, Francisco Javier García
Cenador, María Begoña García
Vicente-Dueñas, Carolina
Hauer, Julia
Ramiro, Almudena R
Sanchez-Garcia, Isidro
Borkhardt, Arndt
author Rodríguez-Hernández, Guillermo
author_facet Rodríguez-Hernández, Guillermo
Opitz, Friederike V
Delgado, Pilar
Walter, Carolin
Alvarez-Prado, Angel Francisco
González-Herrero, Inés
Auer, Franziska
Fischer, Ute
Janssen, Stefan
Bartenhagen, Christoph
Raboso-Gallego, Javier
Casado-García, Ana
Orfao, Alberto
Blanco, Oscar
Alonso-López, Diego
Rivas, Javier De Las
Tena-Dávila, Sara González de
Müschen, Markus
Dugas, Martin
Criado, Francisco Javier García
Cenador, María Begoña García
Vicente-Dueñas, Carolina
Hauer, Julia
Ramiro, Almudena R
Sanchez-Garcia, Isidro
Borkhardt, Arndt
author_role author
author2 Opitz, Friederike V
Delgado, Pilar
Walter, Carolin
Alvarez-Prado, Angel Francisco
González-Herrero, Inés
Auer, Franziska
Fischer, Ute
Janssen, Stefan
Bartenhagen, Christoph
Raboso-Gallego, Javier
Casado-García, Ana
Orfao, Alberto
Blanco, Oscar
Alonso-López, Diego
Rivas, Javier De Las
Tena-Dávila, Sara González de
Müschen, Markus
Dugas, Martin
Criado, Francisco Javier García
Cenador, María Begoña García
Vicente-Dueñas, Carolina
Hauer, Julia
Ramiro, Almudena R
Sanchez-Garcia, Isidro
Borkhardt, Arndt
author2_role author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
dc.contributor.none.fl_str_mv Unión Europea. Fondo Europeo de Desarrollo Regional (FEDER/ERDF)
Instituto de Salud Carlos III
German Cancer Consortium (Alemania)
Unión Europea. Comisión Europea
Unión Europea. Comisión Europea. European Research Council (ERC)
Ministerio de Ciencia, Innovación y Universidades (España)
Fundación ProCNIC
Deutsche Forschungsgemeinschaft (Alemania)
Junta de Castilla y León (España)

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 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.
publishDate 2019
dc.date.none.fl_str_mv 2019
2019-12-05
2019
2019-12-05
2020
2020-01-29
dc.type.none.fl_str_mv journal article
http://purl.org/coar/resource_type/c_6501
VoR
http://purl.org/coar/version/c_970fb48d4fbd8a85
dc.type.openaire.fl_str_mv info:eu-repo/semantics/article
format article
dc.identifier.none.fl_str_mv http://hdl.handle.net/20.500.12105/8953
url http://hdl.handle.net/20.500.12105/8953
dc.language.none.fl_str_mv Inglés
eng
language_invalid_str_mv Inglés
language eng
dc.relation.none.fl_str_mv ES SEV-2015-0505 Not available
European Commission http://dx.doi.org/10.13039/501100000780 Seventh Framework Programme 207844
dc.rights.none.fl_str_mv open access
http://purl.org/coar/access_right/c_abf2
Atribución 4.0 Internacional
http://creativecommons.org/licenses/by/4.0/
dc.rights.openaire.fl_str_mv info:eu-repo/semantics/openAccess
rights_invalid_str_mv open access
http://purl.org/coar/access_right/c_abf2
Atribución 4.0 Internacional
http://creativecommons.org/licenses/by/4.0/
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
application/pdf
application/pdf
application/pdf
application/vnd.openxmlformats-officedocument.spreadsheetml.sheet
application/vnd.openxmlformats-officedocument.spreadsheetml.sheet
dc.publisher.none.fl_str_mv Springer
publisher.none.fl_str_mv Springer
dc.source.none.fl_str_mv reponame:Repisalud
instname:Instituto de Salud Carlos III (ISCIII)
instname_str Instituto de Salud Carlos III (ISCIII)
reponame_str Repisalud
collection Repisalud
repository.name.fl_str_mv
repository.mail.fl_str_mv
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