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Clinical relevance of the tumor microenvironment and immune escape of oral squamous cell carcinoma

BACKGROUND: Changes in the tumor microenvironment and immune surveillance represent crucial hallmarks of various kinds of cancer, including oral squamous cell carcinoma (OSCC), and a close crosstalk of hypoxia regulating genes, an activation of chemokines and immune cells has been described. METHODS...

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Autores principales: Eckert, Alexander W., Wickenhauser, Claudia, Salins, Paul C., Kappler, Matthias, Bukur, Juergen, Seliger, Barbara
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4820994/
https://www.ncbi.nlm.nih.gov/pubmed/27044404
http://dx.doi.org/10.1186/s12967-016-0828-6
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author Eckert, Alexander W.
Wickenhauser, Claudia
Salins, Paul C.
Kappler, Matthias
Bukur, Juergen
Seliger, Barbara
author_facet Eckert, Alexander W.
Wickenhauser, Claudia
Salins, Paul C.
Kappler, Matthias
Bukur, Juergen
Seliger, Barbara
author_sort Eckert, Alexander W.
collection PubMed
description BACKGROUND: Changes in the tumor microenvironment and immune surveillance represent crucial hallmarks of various kinds of cancer, including oral squamous cell carcinoma (OSCC), and a close crosstalk of hypoxia regulating genes, an activation of chemokines and immune cells has been described. METHODS: A review about the pivotal role of HIF-1, its crosstalk to various cornerstones in OSCC tumorigenesis is presented. RESULTS: Hypoxia is a frequent event in OSCC and leads to a reprogramming of the cellular metabolism in order to prevent cell death. Hypoxic OSCC cells induce different adaptive changes such as anaerobic glycolysis, pH stabilisation and alterations of the gene and protein expression profile. This complex metabolic program is orchestrated by the hypoxia inducible factor (HIF)-1, the master regulator of early tumor progression. Hypoxia-dependent and -independent alterations in immune surveillance lead to different immune evasion strategies, which are partially mediated by alterations of the tumor cells, changes in the frequency, activity and repertoire of immune cell infiltrates and of soluble and environmental factors of the tumor micromilieu with consecutive generation of an immune escape phenotype, progression of disease and poor clinical outcome of OSCC patients. CONCLUSIONS: This review focusses on the importance of HIF-1 in the adaption and reprogramming of the metabolic system to reduced oxygen values as well as on the role of the tumor microenvironment for evasion of OSCC from immune recognition and destruction.
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spelling pubmed-48209942016-04-06 Clinical relevance of the tumor microenvironment and immune escape of oral squamous cell carcinoma Eckert, Alexander W. Wickenhauser, Claudia Salins, Paul C. Kappler, Matthias Bukur, Juergen Seliger, Barbara J Transl Med Review BACKGROUND: Changes in the tumor microenvironment and immune surveillance represent crucial hallmarks of various kinds of cancer, including oral squamous cell carcinoma (OSCC), and a close crosstalk of hypoxia regulating genes, an activation of chemokines and immune cells has been described. METHODS: A review about the pivotal role of HIF-1, its crosstalk to various cornerstones in OSCC tumorigenesis is presented. RESULTS: Hypoxia is a frequent event in OSCC and leads to a reprogramming of the cellular metabolism in order to prevent cell death. Hypoxic OSCC cells induce different adaptive changes such as anaerobic glycolysis, pH stabilisation and alterations of the gene and protein expression profile. This complex metabolic program is orchestrated by the hypoxia inducible factor (HIF)-1, the master regulator of early tumor progression. Hypoxia-dependent and -independent alterations in immune surveillance lead to different immune evasion strategies, which are partially mediated by alterations of the tumor cells, changes in the frequency, activity and repertoire of immune cell infiltrates and of soluble and environmental factors of the tumor micromilieu with consecutive generation of an immune escape phenotype, progression of disease and poor clinical outcome of OSCC patients. CONCLUSIONS: This review focusses on the importance of HIF-1 in the adaption and reprogramming of the metabolic system to reduced oxygen values as well as on the role of the tumor microenvironment for evasion of OSCC from immune recognition and destruction. BioMed Central 2016-04-05 /pmc/articles/PMC4820994/ /pubmed/27044404 http://dx.doi.org/10.1186/s12967-016-0828-6 Text en © Eckert et al. 2016 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Review
Eckert, Alexander W.
Wickenhauser, Claudia
Salins, Paul C.
Kappler, Matthias
Bukur, Juergen
Seliger, Barbara
Clinical relevance of the tumor microenvironment and immune escape of oral squamous cell carcinoma
title Clinical relevance of the tumor microenvironment and immune escape of oral squamous cell carcinoma
title_full Clinical relevance of the tumor microenvironment and immune escape of oral squamous cell carcinoma
title_fullStr Clinical relevance of the tumor microenvironment and immune escape of oral squamous cell carcinoma
title_full_unstemmed Clinical relevance of the tumor microenvironment and immune escape of oral squamous cell carcinoma
title_short Clinical relevance of the tumor microenvironment and immune escape of oral squamous cell carcinoma
title_sort clinical relevance of the tumor microenvironment and immune escape of oral squamous cell carcinoma
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4820994/
https://www.ncbi.nlm.nih.gov/pubmed/27044404
http://dx.doi.org/10.1186/s12967-016-0828-6
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