Publication:
Macrophages, inflammation, and tumor suppressors: ARF, a new player in the game

dc.contributor.authorTravés, Paqui G
dc.contributor.authorLuque, Alfonso
dc.contributor.authorHortelano, Sonsoles
dc.contributor.funderInstituto de Salud Carlos III
dc.date.accessioned2018-11-15T09:59:59Z
dc.date.available2018-11-15T09:59:59Z
dc.date.issued2012
dc.description.abstractThe interaction between tumor progression and innate immune system has been well established in the last years. Indeed, several lines of clinical evidence indicate that immune cells such as tumor-associated macrophages (TAMs) interact with tumor cells, favoring growth, angiogenesis, and metastasis of a variety of cancers. In most tumors, TAMs show properties of an alternative polarization phenotype (M2) characterized by the expression of a series of chemokines, cytokines, and proteases that promote immunosuppression, tumor proliferation, and spreading of the cancer cells. Tumor suppressor genes have been traditionally linked to the regulation of cancer progression; however, a growing body of evidence indicates that these genes also play essential roles in the regulation of innate immunity pathways through molecular mechanisms that are still poorly understood. In this paper, we provide an overview of the immunobiology of TAMs as well as what is known about tumor suppressors in the context of immune responses. Recent advances regarding the role of the tumor suppressor ARF as a regulator of inflammation and macrophage polarization are also reviewed.es_ES
dc.description.sponsorshipThis study was supported by Grants PI11.0036 from the FIS and MPY 1410/09 from ISCIII to S. Hortelano.es_ES
dc.format.volume2012es_ES
dc.identifier.citationMediators Inflamm. 2012; Article ID:568783.es_ES
dc.identifier.doi10.1155/2012/568783es_ES
dc.identifier.e-issn1466-1861es_ES
dc.identifier.issn0962-9351es_ES
dc.identifier.journalMediators of inflammationes_ES
dc.identifier.pubmedID23316105es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/6594
dc.language.isoenges_ES
dc.publisherHindawi
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/PI11.0036es_ES
dc.relation.publisherversionhttps://www.doi.org/10.1155/2012/568783es_ES
dc.repisalud.centroISCIII::Centro Nacional de Microbiología (CNM)es_ES
dc.repisalud.institucionISCIIIes_ES
dc.rights.accessRightsopen accesses_ES
dc.rights.licenseAtribución-3.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/*
dc.subject.meshAnimalses_ES
dc.subject.meshCyclin-Dependent Kinase Inhibitor p16es_ES
dc.subject.meshHumanses_ES
dc.subject.meshImmune Tolerancees_ES
dc.subject.meshInflammation Mediatorses_ES
dc.subject.meshMacrophageses_ES
dc.subject.meshNeoplasmses_ES
dc.subject.meshNeovascularization, Pathologices_ES
dc.subject.meshTumor Microenvironmentes_ES
dc.subject.meshTumor Suppressor Protein p14ARFes_ES
dc.subject.meshTumor Suppressor Proteinses_ES
dc.titleMacrophages, inflammation, and tumor suppressors: ARF, a new player in the gamees_ES
dc.typeresearch articlees_ES
dc.type.hasVersionVoRes_ES
dspace.entity.typePublication
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