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DC Field | Value | Language |
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dc.contributor.author | Sistigu, A | - |
dc.contributor.author | Yamazaki, T | - |
dc.contributor.author | Vacchelli, E | - |
dc.contributor.author | Chaba, Kariman | - |
dc.contributor.author | Enot, D.P | - |
dc.contributor.author | Adam, J | - |
dc.contributor.author | Vitale, I | - |
dc.contributor.author | Goubar, A | - |
dc.contributor.author | Baracco, E.E | - |
dc.contributor.author | Remedios, C | - |
dc.contributor.author | Fend, L | - |
dc.contributor.author | Hannani, D | - |
dc.contributor.author | Aymeric, L | - |
dc.contributor.author | Ma, Y | - |
dc.contributor.author | Niso Santano, Mireia | - |
dc.contributor.author | Kepp, O | - |
dc.contributor.author | Schultze, J.L | - |
dc.contributor.author | Tuting, T | - |
dc.contributor.author | Belardelli, F | - |
dc.contributor.author | Bracci, L | - |
dc.contributor.author | La Sorsa, V | - |
dc.contributor.author | Ziccheddu, G | - |
dc.contributor.author | Sestili, P | - |
dc.contributor.author | Urbani, F | - |
dc.contributor.author | Delorenzi, M | - |
dc.contributor.author | Lacroix Triki, M | - |
dc.contributor.author | Quidville, V | - |
dc.contributor.author | Conforti, R | - |
dc.contributor.author | Spano, J.P | - |
dc.contributor.author | Pusztai, L | - |
dc.contributor.author | Poirier Colame, V | - |
dc.contributor.author | Delaloge, S | - |
dc.contributor.author | Penault Llorca, F | - |
dc.contributor.author | Ladoire, S | - |
dc.contributor.author | Arnould, L | - |
dc.contributor.author | Cyrta, J | - |
dc.contributor.author | Dessoliers, M.C | - |
dc.contributor.author | Eggermont, A | - |
dc.contributor.author | Bianchi, M.J | - |
dc.contributor.author | Pittet, M | - |
dc.contributor.author | Engblom, C | - |
dc.contributor.author | Pfirschke, C | - |
dc.contributor.author | Preville, X | - |
dc.contributor.author | Uze, G | - |
dc.contributor.author | Schreiber, R.D | - |
dc.contributor.author | Chow, M.T | - |
dc.contributor.author | Smyth, M.J | - |
dc.contributor.author | Proietti, E | - |
dc.contributor.author | Andre, F | - |
dc.contributor.author | Kroemer, Guido | - |
dc.contributor.author | Zitvogel, L | - |
dc.date.accessioned | 2024-02-02T11:56:38Z | - |
dc.date.available | 2024-02-02T11:56:38Z | - |
dc.date.issued | 2014 | - |
dc.identifier.uri | http://hdl.handle.net/10662/19776 | - |
dc.description.abstract | Some of the anti-neoplastic effects of anthracyclines in mice originate from the induction of innate and T cell–mediated anticancer immune responses. Here we demonstrate that anthracyclines stimulate the rapid production of type I interferons (IFNs) by malignant cells after activation of the endosomal pattern recognition receptor Toll-like receptor 3 (TLR3). By binding to IFN-α and IFN-β receptors (IFNARs) on neoplastic cells, type I IFNs trigger autocrine and paracrine circuitries that result in the release of chemokine (C-X-C motif) ligand 10 (CXCL10). Tumors lacking Tlr3 or Ifnar failed to respond to chemotherapy unless type I IFN or Cxcl10, respectively, was artificially supplied. Moreover, a type I IFN–related signature predicted clinical responses to anthracycline-based chemotherapy in several independent cohorts of patients with breast carcinoma characterized by poor prognosis. Our data suggest that anthracycline-mediated immune responses mimic those induced by viral pathogens. We surmise that such 'viral mimicry' constitutes a hallmark of successful chemotherapy. | es_ES |
dc.description.abstract | Algunos de los efectos antineoplásicos de las antraciclinas en ratones tienen su origen en la inducción de respuestas inmunitarias innatas y mediadas por células T contra el cáncer. Aquí demostramos que las antraciclinas estimulan la rápida producción de interferones de tipo I (IFN) por parte de las células malignas tras la activación del receptor endosomal de reconocimiento de patrones Toll-like receptor 3 (TLR3). Al unirse a los receptores IFN-α e IFN-β (IFNAR) de las células neoplásicas, los IFN de tipo I desencadenan circuitos autocrinos y paracrinos que dan lugar a la liberación del ligando 10 de quimiocinas (motivo C-X-C) (CXCL10). Los tumores que carecen de Tlr3 o Ifnar no responden a la quimioterapia a menos que se les suministre artificialmente IFN de tipo I o Cxcl10, respectivamente. Además, una firma relacionada con el IFN tipo I predijo las respuestas clínicas a la quimioterapia basada en antraciclinas en varias cohortes independientes de pacientes con carcinoma de mama caracterizado por un mal pronóstico. Nuestros datos sugieren que las respuestas inmunitarias mediadas por antraciclinas imitan las inducidas por patógenos virales. Suponemos que este "mimetismo viral" constituye una característica distintiva del éxito de la quimioterapia. | es_ES |
dc.description.sponsorship | We acknowledge L. Galluzzi for help with preparation of the manuscript. We thank P. Rameau, Y. Lécluse and M. Sanchez for assistance with FACS experiments, G. Schiavoni and G. D'Agostino (Istituto Superiore di Sanità) for recombinant Ifn-α1, our colleagues from the Gustave Roussy Cancer Center and the Istituto Superiore di Sanità animal facilities, P. Gonin, M. Macchia and E. Cardarelli. We acknowledge P. Vielh for his help with immunohistochemical analyses and G. Stoll for his support in statistical analyses. G.K. and L.Z. are supported by the Ligue Nationale contre le Cancer (Equipes labellisées), Site de Recherche Intégrée sur le Cancer (IRIC) Socrates, the ISREC Foundation, Agence Nationale pour la Recherche (ANR AUTOPH, ANR Emergence), the European Commission (ArtForce), a European Research Council Advanced Investigator Grant (to G.K.), the Fondation pour la Recherche Médicale (FRM), the Institut National du Cancer (INCa), the Fondation de France, Cancéropôle Ile-de-France, the Fondation Bettencourt-Schueller, the LabEx Immuno-Oncology and the Paris Alliance of Cancer Research Institutes. A.S. is supported by Ligue Nationale contre le Cancer. D.H. was supported by Fondation Association pour la Recherche sur le Cancer. M.J.S. was supported by a National Health and Medical Research Council (NH&MRC) Australia Fellowship and Program Grant and a grant from the Victorian Cancer Agency. E.P. and L.B. were supported by Associazione Italiana Ricerca contro il Cancro (AIRC) (MFAG_13058). C.P. was supported by the Deutsche Forschungsgemeinschaft (DFG) PF809/1-1. C.E. was supported by Boerhinger Ingelheim. F.A. was supported by Association Vie et Cancer. J.A. was supported by Institut national du Cancer et la Direction Générale de l′Offre de Soins-INSERM 6043. | - |
dc.format.extent | 12 p. | es_ES |
dc.format.mimetype | application/pdf | en_US |
dc.language.iso | eng | es_ES |
dc.publisher | Nature Research | es_ES |
dc.subject | Cáncer | es_ES |
dc.subject | Cancer | en_US |
dc.subject | Interferon tipo I | es_ES |
dc.subject | Type I interferon | en_US |
dc.subject | TLR3 | es_ES |
dc.title | Cancer cell–autonomous contribution of type I interferon signaling to the efficacy of chemotherapy | es_ES |
dc.type | article | es_ES |
dc.description.version | peerReviewed | es_ES |
europeana.type | TEXT | en_US |
dc.rights.accessRights | closedAccess | es_ES |
dc.subject.unesco | 32 Ciencias Médicas | es_ES |
dc.subject.unesco | 24 Ciencias de la Vida | es_ES |
europeana.dataProvider | Universidad de Extremadura. España | es_ES |
dc.identifier.bibliographicCitation | Sistigu, A., Yamazaki, T., Vacchelli, E., Chaba, K., Eno, D.P., Adam, J., Vitale, I., Goubar, A., Baracco, E.E., Remédios, C., Fend, L., Hannani, D., Aymeric, L., Ma, Y., Niso-Santano, M., Kepp, O., Schultze, J.L., Tüting, T., Belardelli, F., Bracci, L., La Sorsa, V., Ziccheddu, G., Sestili, P., Urbani, F., Delorenzi, M., Lacroix-Triki, M., Quidville, V., Conforti, R., Spano, J.P., Puszta,i L., Poirier-Colame, V., Delaloge, S., Penault-Llorca, F., Ladoire, S., Arnould, L., Cyrta, J., Dessoliers, M.C., Eggermont, A., Bianchi, M.E., Pittet, M., Engblom, C., Pfirschke, C., Préville, X., Uzè, G., Schreiber, R.D., Chow, M.T., Smyth, M.J., Proietti, E., André, F., Kroemer, G., Zitvogel, L. Cancer cell-autonomous contribution of type I interferon signaling to the efficacy of chemotherapy. ( 2014). Nature Medicine, 20(11), 1301-1309. https://doi.org/10.1038/nm.3708 | es_ES |
dc.type.version | publishedVersion | es_ES |
dc.contributor.affiliation | Universidad de Extremadura. Departamento de Bioquímica, Biología Molecular y Genética | es_ES |
dc.contributor.affiliation | Université Paris Saclay. France | - |
dc.contributor.affiliation | Université Paris-Sorbonne (Paris I). France | - |
dc.relation.publisherversion | https://www.nature.com/articles/nm.3708 | es_ES |
dc.identifier.doi | 10.1038/nm.3708 | - |
dc.identifier.publicationtitle | Nature Medicine | es_ES |
dc.identifier.publicationissue | 20 | es_ES |
dc.identifier.publicationfirstpage | 1301 | es_ES |
dc.identifier.publicationlastpage | 1309 | es_ES |
dc.identifier.publicationvolume | 11 | es_ES |
dc.identifier.orcid | 0000-0002-6506-422X | es_ES |
Appears in Collections: | DBYBM - Artículos |
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