Immune Evasion in Pancreatic Cancer: From Mechanisms to Therapy

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• dc.contributor.author Martínez Bosch, Neusca
• dc.contributor.author Vinaixa Forner, Judith, 1991-ca
• dc.contributor.author Navarro Medrano, Pilarca
• dc.date.accessioned 2018-10-22T07:34:04Z
• dc.date.available 2018-10-22T07:34:04Z
• dc.date.issued 2018
• 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.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.doi http://dx.doi.org/10.3390/cancers10010006
• dc.identifier.issn 2072-6694
• dc.identifier.uri http://hdl.handle.net/10230/35627
• dc.language.iso eng
• dc.publisher MDPIca
• dc.relation.ispartof Cancers (Basel). 2018 Jan 3;10(1):E6
• 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.accessRights info:eu-repo/semantics/openAccess
• dc.rights.uri http://creativecommons.org/licenses/by/4.0/
• 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.subject.other Immunoteràpia
• dc.subject.other Pàncrees -- Càncer
• dc.title Immune Evasion in Pancreatic Cancer: From Mechanisms to Therapyca
• dc.type info:eu-repo/semantics/article
• dc.type.version info:eu-repo/semantics/publishedVersion