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dc.contributor.author Rutkowski, Melanie R.
dc.contributor.author Stephen, Tom L.
dc.contributor.author Svoronos, Nikolaos
dc.contributor.author Allegrezza, Michael J.
dc.contributor.author Tesone, Amelia J.
dc.contributor.author Perales Puchalt, Alfredo
dc.contributor.author Brencicova, Eva
dc.contributor.author Escovar Fadul, Ximena
dc.contributor.author Nguyen, Jenny M.
dc.contributor.author Cadungog, Mark G.
dc.contributor.author Zhang, Rugang
dc.contributor.author Salatino, Mariana
dc.contributor.author Tchou, Julia
dc.contributor.author Rabinovich, Gabriel Adrián
dc.contributor.author Conejo Garcia, Jose R.
dc.date.available 2017-08-24T20:30:13Z
dc.date.issued 2015-01-12
dc.identifier.citation Rutkowski, Melanie R.; Stephen, Tom L.; Svoronos, Nikolaos; Allegrezza, Michael J.; Tesone, Amelia J.; et al.; Microbially driven TLR5-dependent signaling governs distal malignant progression through tumor-promoting inflammation; Cell Press; Cancer Cell; 27; 1; 12-1-2015; 27-40
dc.identifier.issn 1535-6108
dc.identifier.uri http://hdl.handle.net/11336/22973
dc.description.abstract The dominant TLR5(R392X) polymorphism abrogates flagellin responses in >7% of humans. We report that TLR5-dependent commensal bacteria drive malignant progression at extramucosal locations by increasing systemic IL-6, which drives mobilization of myeloid-derived suppressor cells (MDSCs). Mechanistically, expanded granulocytic MDSCs cause γδ lymphocytes in TLR5-responsive tumors to secrete galectin-1, dampening antitumor immunity and accelerating malignant progression. In contrast, IL-17 is consistently upregulated in TLR5-unresponsive tumor-bearing mice but only accelerates malignant progression in IL-6-unresponsive tumors. Importantly, depletion of commensal bacteria abrogates TLR5-dependent differences in tumor growth. Contrasting differences in inflammatory cytokines and malignant evolution are recapitulated in TLR5-responsive/unresponsive ovarian and breast cancer patients. Therefore, inflammation, antitumor immunity, and the clinical outcome of cancer patients are influenced by a common TLR5 polymorphism.
dc.format application/pdf
dc.language.iso eng
dc.publisher Cell Press
dc.rights info:eu-repo/semantics/restrictedAccess
dc.rights.uri https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.subject bacteria
dc.subject TLR5
dc.subject myeloid-derived suppresor cells
dc.subject tumor
dc.subject.classification Bioquímica y Biología Molecular
dc.subject.classification Medicina Básica
dc.subject.classification CIENCIAS MÉDICAS Y DE LA SALUD
dc.title Microbially driven TLR5-dependent signaling governs distal malignant progression through tumor-promoting inflammation
dc.type info:eu-repo/semantics/article
dc.type info:ar-repo/semantics/artículo
dc.type info:eu-repo/semantics/publishedVersion
dc.date.updated 2017-08-08T14:24:43Z
dc.identifier.eissn 1878-3686
dc.journal.volume 27
dc.journal.number 1
dc.journal.pagination 27-40
dc.journal.pais Estados Unidos
dc.journal.ciudad Cambridge
dc.description.fil Fil: Rutkowski, Melanie R.. The Wistar Institute. Tumor Microenvironment and Metastasis Program; Estados Unidos
dc.description.fil Fil: Stephen, Tom L.. The Wistar Institute. Tumor Microenvironment and Metastasis Program; Estados Unidos
dc.description.fil Fil: Svoronos, Nikolaos. The Wistar Institute. Tumor Microenvironment and Metastasis Program; Estados Unidos
dc.description.fil Fil: Allegrezza, Michael J.. The Wistar Institute. Tumor Microenvironment and Metastasis Program; Estados Unidos
dc.description.fil Fil: Tesone, Amelia J.. The Wistar Institute. Tumor Microenvironment and Metastasis Program; Estados Unidos
dc.description.fil Fil: Perales Puchalt, Alfredo. The Wistar Institute. Tumor Microenvironment and Metastasis Program; Estados Unidos
dc.description.fil Fil: Brencicova, Eva. The Wistar Institute. Tumor Microenvironment and Metastasis Program; Estados Unidos
dc.description.fil Fil: Escovar Fadul, Ximena. The Wistar Institute. Tumor Microenvironment and Metastasis Program; Estados Unidos
dc.description.fil Fil: Nguyen, Jenny M.. The Wistar Institute. Tumor Microenvironment and Metastasis Program; Estados Unidos
dc.description.fil Fil: Cadungog, Mark G.. Christiana Care Health System. Helen F. Graham Cancer Center; Estados Unidos
dc.description.fil Fil: Zhang, Rugang. The Wistar Institute. Gene Expression and Regulation Program; Estados Unidos
dc.description.fil Fil: Salatino, Mariana. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina
dc.description.fil Fil: Tchou, Julia. University of Pennsylvania; Estados Unidos
dc.description.fil Fil: Rabinovich, Gabriel Adrián. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina
dc.description.fil Fil: Conejo Garcia, Jose R.. The Wistar Institute. Gene Expression and Regulation Program; Estados Unidos
dc.journal.title Cancer Cell
dc.relation.alternativeid info:eu-repo/semantics/altIdentifier/url/http://www.cell.com/cancer-cell/fulltext/S1535-6108(14)00460-7
dc.relation.alternativeid info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1016/j.ccell.2014.11.009
dc.relation.alternativeid info:eu-repo/semantics/altIdentifier/pmid/25533336
dc.relation.alternativeid info:eu-repo/semantics/altIdentifier/url/https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4293269/


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info:eu-repo/semantics/restrictedAccess Excepto donde se diga explícitamente, este item se publica bajo la siguiente descripción: Creative Commons Attribution-NonCommercial-ShareAlike 2.5 Unported (CC BY-NC-SA 2.5)