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Immune Evasion in Pancreatic Cancer: From Mechanisms to Therapy

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dc.contributor.author Martínez Bosch, Neus
dc.contributor.author Vinaixa, Judith
dc.contributor.author Navarro Medrano, Pilar
dc.date.accessioned 2018-10-22T07:34:04Z
dc.date.available 2018-10-22T07:34:04Z
dc.date.issued 2018
dc.identifier.citation Martinez-Bosch N, Vinaixa J, Navarro P. Immune Evasion in Pancreatic Cancer: From Mechanisms to Therapy. Cancers (Basel). 2018 Jan 3;10(1). pii: E6. DOI: 10.3390/cancers10010006
dc.identifier.issn 2072-6694
dc.identifier.uri http://hdl.handle.net/10230/35627
dc.description.abstract Pancreatic ductal adenocarcinoma (PDA), the most frequent type of pancreatic cancer, remains one of the most challenging problems for the biomedical and clinical fields, with abysmal survival rates and poor therapy efficiency. Desmoplasia, which is abundant in PDA, can be blamed for much of the mechanisms behind poor drug performance, as it is the main source of the cytokines and chemokines that orchestrate rapid and silent tumor progression to allow tumor cells to be isolated into an extensive fibrotic reaction, which results in inefficient drug delivery. However, since immunotherapy was proclaimed as the breakthrough of the year in 2013, the focus on the stroma of pancreatic cancer has interestingly moved from activated fibroblasts to the immune compartment, trying to understand the immunosuppressive factors that play a part in the strong immune evasion that characterizes PDA. The PDA microenvironment is highly immunosuppressive and is basically composed of T regulatory cells (Tregs), tumor-associated macrophages (TAMs), and myeloid-derived suppressive cells (MDSCs), which block CD8⁺ T-cell duties in tumor recognition and clearance. Interestingly, preclinical data have highlighted the importance of this immune evasion as the source of resistance to single checkpoint immunotherapies and cancer vaccines and point at pathways that inhibit the immune attack as a key to solve the therapy puzzle. Here, we will discuss the molecular mechanisms involved in PDA immune escape as well as the state of the art of the PDA immunotherapy.
dc.format.mimetype application/pdf
dc.language.iso eng
dc.publisher MDPI
dc.rights Copyright © 2018 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
dc.rights.uri http://creativecommons.org/licenses/by/4.0/
dc.subject.other Immunoteràpia
dc.subject.other Pàncrees -- Càncer
dc.title Immune Evasion in Pancreatic Cancer: From Mechanisms to Therapy
dc.type info:eu-repo/semantics/article
dc.identifier.doi http://dx.doi.org/10.3390/cancers10010006
dc.subject.keyword Galectins
dc.subject.keyword Immune checkpoints
dc.subject.keyword Immune surveillance
dc.subject.keyword Immunotherapy
dc.subject.keyword Pancreatic cancer
dc.subject.keyword Stroma
dc.rights.accessRights info:eu-repo/semantics/openAccess
dc.type.version info:eu-repo/semantics/publishedVersion

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