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Dysregulation of signaling pathways associated with innate antibacterial immunity in patients with pancreatic cancer
Disorders of innate antibacterial response are of fundamental importance in the development of gastrointestinal cancers, including pancreatic cancer. Multi-regulatory properties of the Toll-like receptors (TLRs) (e.g., regulation of proliferation, the activity of NF-κB, gene transcription of apoptos...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Polish Society of Experimental and Clinical Immunology
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5382886/ https://www.ncbi.nlm.nih.gov/pubmed/28450804 http://dx.doi.org/10.5114/ceji.2016.65140 |
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author | Słotwiński, Robert Słotwińska, Sylwia Małgorzata |
author_facet | Słotwiński, Robert Słotwińska, Sylwia Małgorzata |
author_sort | Słotwiński, Robert |
collection | PubMed |
description | Disorders of innate antibacterial response are of fundamental importance in the development of gastrointestinal cancers, including pancreatic cancer. Multi-regulatory properties of the Toll-like receptors (TLRs) (e.g., regulation of proliferation, the activity of NF-κB, gene transcription of apoptosis proteins, regulation of angiogenesis, HIF-1α protein expression) are used in experimental studies to better understand the pathogenesis of pancreatic cancer, for early diagnosis, and for more effective therapeutic intervention. There are known numerous examples of TLR agonists (e.g., TLR2/5 ligands, TLR6, TLR9) of antitumor effect. The direction of these studies is promising, but a small number of them does not allow for an accurate assessment of the impact of TLR expression disorders, proteins of these signaling pathways, or attempts to block or stimulate them, on the results of treatment of pancreatic cancer patients. It is known, however, that the expression disorders of proteins of innate antibacterial response signaling pathways occur not only in tumor tissue but also in peripheral blood leukocytes of pancreatic cancer patients (e.g., increased expression of TLR4, NOD1, TRAF6), which is one of the most important factors facilitating further tumor development. This review mainly focuses on the genetic aspects of signaling pathway disorders associated with innate antibacterial response in the pathogenesis and diagnosis of pancreatic cancer. |
format | Online Article Text |
id | pubmed-5382886 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Polish Society of Experimental and Clinical Immunology |
record_format | MEDLINE/PubMed |
spelling | pubmed-53828862017-04-27 Dysregulation of signaling pathways associated with innate antibacterial immunity in patients with pancreatic cancer Słotwiński, Robert Słotwińska, Sylwia Małgorzata Cent Eur J Immunol Review Paper Disorders of innate antibacterial response are of fundamental importance in the development of gastrointestinal cancers, including pancreatic cancer. Multi-regulatory properties of the Toll-like receptors (TLRs) (e.g., regulation of proliferation, the activity of NF-κB, gene transcription of apoptosis proteins, regulation of angiogenesis, HIF-1α protein expression) are used in experimental studies to better understand the pathogenesis of pancreatic cancer, for early diagnosis, and for more effective therapeutic intervention. There are known numerous examples of TLR agonists (e.g., TLR2/5 ligands, TLR6, TLR9) of antitumor effect. The direction of these studies is promising, but a small number of them does not allow for an accurate assessment of the impact of TLR expression disorders, proteins of these signaling pathways, or attempts to block or stimulate them, on the results of treatment of pancreatic cancer patients. It is known, however, that the expression disorders of proteins of innate antibacterial response signaling pathways occur not only in tumor tissue but also in peripheral blood leukocytes of pancreatic cancer patients (e.g., increased expression of TLR4, NOD1, TRAF6), which is one of the most important factors facilitating further tumor development. This review mainly focuses on the genetic aspects of signaling pathway disorders associated with innate antibacterial response in the pathogenesis and diagnosis of pancreatic cancer. Polish Society of Experimental and Clinical Immunology 2017-01-24 2016 /pmc/articles/PMC5382886/ /pubmed/28450804 http://dx.doi.org/10.5114/ceji.2016.65140 Text en Copyright: © 2017 Polish Society of Experimental and Clinical Immunology http://creativecommons.org/licenses/by-nc-sa/4.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) License, allowing third parties to copy and redistribute the material in any medium or format and to remix, transform, and build upon the material, provided the original work is properly cited and states its license. |
spellingShingle | Review Paper Słotwiński, Robert Słotwińska, Sylwia Małgorzata Dysregulation of signaling pathways associated with innate antibacterial immunity in patients with pancreatic cancer |
title | Dysregulation of signaling pathways associated with innate antibacterial immunity in patients with pancreatic cancer |
title_full | Dysregulation of signaling pathways associated with innate antibacterial immunity in patients with pancreatic cancer |
title_fullStr | Dysregulation of signaling pathways associated with innate antibacterial immunity in patients with pancreatic cancer |
title_full_unstemmed | Dysregulation of signaling pathways associated with innate antibacterial immunity in patients with pancreatic cancer |
title_short | Dysregulation of signaling pathways associated with innate antibacterial immunity in patients with pancreatic cancer |
title_sort | dysregulation of signaling pathways associated with innate antibacterial immunity in patients with pancreatic cancer |
topic | Review Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5382886/ https://www.ncbi.nlm.nih.gov/pubmed/28450804 http://dx.doi.org/10.5114/ceji.2016.65140 |
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