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dc.contributor.authorSchönhuber, Ninaes_ES
dc.contributor.authorSeidler, Barbaraes_ES
dc.contributor.authorSchuck, Kathleenes_ES
dc.contributor.authorVeltkamp, Christianes_ES
dc.contributor.authorSchachtler, Christinaes_ES
dc.contributor.authorZukowska, Magdalenaes_ES
dc.contributor.authorEser, Stefanes_ES
dc.contributor.authorFeyerabend, Thorsten Bes_ES
dc.contributor.authorPaul, Mariel Ces_ES
dc.contributor.authorEser, Philippes_ES
dc.contributor.authorKlein, Sabinees_ES
dc.contributor.authorLowy, Andrew Mes_ES
dc.contributor.authorBanergee, Rubyes_ES
dc.contributor.authorYan, Fangtanges_ES
dc.contributor.authorLee, Chang-Lunges_ES
dc.contributor.authorModing, Everett Jes_ES
dc.contributor.authorKirsch, David Ges_ES
dc.contributor.authorScheideler, Angelikaes_ES
dc.contributor.authorAlessi, Dario Res_ES
dc.contributor.authorVarela Egocheaga, Ignacio es_ES
dc.contributor.authorBradley, Allanes_ES
dc.contributor.authorKind, Alexanderes_ES
dc.contributor.authorSchnieke, Angelika Ees_ES
dc.contributor.authorRodewald, Hans Reimeres_ES
dc.contributor.authorRad, Rolandes_ES
dc.contributor.authorSchmid, Roland Mes_ES
dc.contributor.authorSchneider, Günteres_ES
dc.contributor.authorSaur, Dieteres_ES
dc.contributor.otherUniversidad de Cantabriaes_ES
dc.date.accessioned2016-11-28T12:52:18Z
dc.date.available2016-11-28T12:52:18Z
dc.date.issued2014es_ES
dc.identifier.issn1078-8956es_ES
dc.identifier.issn1546-170Xes_ES
dc.identifier.urihttp://hdl.handle.net/10902/9717
dc.description.abstractGenetically engineered mouse models (GEMMs) have dramatically improved our understanding of tumor evolution and therapeutic resistance. However, sequential genetic manipulation of gene expression and targeting of the host is almost impossible using conventional Cre-loxP-based models. We have developed an inducible dual-recombinase system by combining flippase-FRT (Flp-FRT) and Cre-loxP recombination technologies to improve GEMMs of pancreatic cancer. This enables investigation of multistep carcinogenesis, genetic manipulation of tumor subpopulations (such as cancer stem cells), selective targeting of the tumor microenvironment and genetic validation of therapeutic targets in autochthonous tumors on a genome-wide scale. As a proof of concept, we performed tumor cell-autonomous and nonautonomous targeting, recapitulated hallmarks of human multistep carcinogenesis, validated genetic therapy by 3-phosphoinositide-dependent protein kinase inactivation as well as cancer cell depletion and show that mast cells in the tumor microenvironment, which had been thought to be key oncogenic players, are dispensable for tumor formationes_ES
dc.format.extent8 p.es_ES
dc.language.isoenges_ES
dc.sourceNat Med. 2014 Nov;20(11):1340-7es_ES
dc.titleA next-generation dual-recombinase system for time- and host-specific targeting of pancreatic canceres_ES
dc.typeinfo:eu-repo/semantics/articlees_ES
dc.rights.accessRightsopenAccesses_ES
dc.identifier.DOI10.1038/nm.3646es_ES
dc.type.versionpublishedVersiones_ES


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