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Pancreatitis-induced inflammation contributes to pancreatic cancer by inhibiting oncogene-induced senescence.

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dc.contributor.authorGuerra, Carmen
dc.contributor.authorCollado, Manuel
dc.contributor.authorNavas, Carolina
dc.contributor.authorSchuhmacher, Alberto J
dc.contributor.authorHernández-Porras, Isabel
dc.contributor.authorCañamero, Marta
dc.contributor.authorRodriguez-Justo, Manuel
dc.contributor.authorSerrano, Manuel
dc.contributor.authorBarbacid, Mariano
dc.contributor.funderUnión Europea. Comisión Europea. European Research Council (ERC)
dc.contributor.funderComunidad de Madrid (España)
dc.contributor.funderMinisterio de Ciencia y Competitividad (España)
dc.contributor.funderMarcelino Botin Foundationes_ES
dc.contributor.funderUCLH/UCL Comprehensive Biomedical Research Centre (London, UK)es_ES
dc.date.accessioned2024-09-16T08:16:54Z
dc.date.available2024-09-16T08:16:54Z
dc.date.issued2011-06-14
dc.description.abstractPancreatic acinar cells of adult mice (?P60) are resistant to transformation by some of the most robust oncogenic insults including expression of K-Ras oncogenes and loss of p16Ink4a/p19Arf or Trp53 tumor suppressors. Yet, these acinar cells yield pancreatic intraepithelial neoplasias (mPanIN) and ductal adenocarcinomas (mPDAC) if exposed to limited bouts of non-acute pancreatitis, providing they harbor K-Ras oncogenes. Pancreatitis contributes to tumor progression by abrogating the senescence barrier characteristic of low-grade mPanINs. Attenuation of pancreatitis-induced inflammation also accelerates tissue repair and thwarts mPanIN expansion. Patients with chronic pancreatitis display senescent PanINs, providing they have received antiinflammatory drugs. These results support the concept that antiinflammatory treatment of people diagnosed with pancreatitis may reduce their risk of developing PDAC.es_ES
dc.description.peerreviewedSíes_ES
dc.description.sponsorshipWe thank I. Aragon, M. Lamparero, M. Lozano, E. Martinez, M. San Roman, and R. Villar for excellent technical assistance. We also value the excellent support provided by V. Alvarez, E. Gil, M. Gomez, P. Gonzalez, and N. Matesanz with histopathology. We thank A. Skoudy (IMIM, Barcelona) for providing the Pdx1 antibody, J.I. Gordon (Washington University School of Medicine, St. Louis, MO) for providing the tetO-PhCMV-Cre mice and Paul Grippo (Northwestern University, Chicago, IL), and Eric Sandgren (University of Wisconsin, Madison, WI) for providing the Elastase-tTA strain. Work in the laboratory of M.B. was supported by grants from the EU-Framework Programme (LSHG-CT-2007-037665), European Research Council (ERC-AG/250297-RAS AHEAD), Spanish Ministry of Science and Innovation (MICINN) (SAF2006-11773 and CSD2007-00017), Autonomous Community of Madrid (GR/SAL/0587/2004 and S2006/BIO-0232) and Fundacion de la Mutua Madrilena del Automovil to M.B and by grants from Fondo de Investigacion Sanitaria (PI042124) and Autonomous Community of Madrid (GR/SAL/0349/2004) to C.G. Work in the laboratory of M.S. was funded by grants from the EU-Framework Programme (PROTEOMAGE), European Research Council (ERC-AG/233270), MICINN (SAF2008-02959 and CSD2007-00017), and the Marcelino Botin Foundation. M.R.-J. is supported by the UCLH/UCL Comprehensive Biomedical Research Centre (London, UK). M.C. is the recipient of a "Ramon y Cajal" contract from the MCINN.es_ES
dc.format.number6es_ES
dc.format.page728es_ES
dc.format.volume19es_ES
dc.identifier.citationCancer Cell . 2011;19(6):728-39es_ES
dc.identifier.doi10.1016/j.ccr.2011.05.011es_ES
dc.identifier.e-issn1878-3686es_ES
dc.identifier.journalCancer celles_ES
dc.identifier.pmchttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4890723/pdf/emss-52291.pdf
dc.identifier.pubmedID21665147es_ES
dc.identifier.urihttps://hdl.handle.net/20.500.12105/23072
dc.language.isoenges_ES
dc.publisherCell Press
dc.relation.projectFECYTinfo:eu-repo/grantAgreement/ES/SAF2006-11773es_ES
dc.relation.projectFECYTinfo:eu-repo/grantAgreement/ES/CSD2007-00017es_ES
dc.relation.projectFECYTinfo:eu-repo/grantAgreement/EC/FP7/250297/EUes_ES
dc.relation.projectFECYTinfo:eu-repo/grantAgreement/EC/FP7/233270/EUes_ES
dc.relation.projectFECYTinfo:eu-repo/grantAgreement/ES/PI042124es_ES
dc.relation.publisherversionhttps://doi.org/10.1016/j.ccr.2011.05.011es_ES
dc.repisalud.institucionCNIOes_ES
dc.repisalud.orgCNIOCNIO::Grupos de investigación::Grupo de Oncología Experimentales_ES
dc.rights.accessRightsopen accesses_ES
dc.rights.licenseAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subject.meshCellular Senescencees_ES
dc.subject.meshGenes, rases_ES
dc.subject.meshAdenocarcinomaes_ES
dc.subject.meshAnimalses_ES
dc.subject.meshAnti-Inflammatory Agentses_ES
dc.subject.meshCarcinoma, Pancreatic Ductales_ES
dc.subject.meshCell Transformation, Neoplastices_ES
dc.subject.meshCyclin-Dependent Kinase Inhibitor p16es_ES
dc.subject.meshGenes, p53es_ES
dc.subject.meshHumanses_ES
dc.subject.meshMicees_ES
dc.subject.meshPancreas, Exocrinees_ES
dc.subject.meshPancreatic Neoplasmses_ES
dc.subject.meshPancreatitises_ES
dc.titlePancreatitis-induced inflammation contributes to pancreatic cancer by inhibiting oncogene-induced senescence.es_ES
dc.typeresearch articlees_ES
dc.type.hasVersionAMes_ES
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