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Exploiting inflammation for therapeutic gain in pancreatic cancer

Pancreatic ductal adenocarcinoma (PDAC) is an aggressive malignancy associated with <5% 5-year survival, in which standard chemotherapeutics have limited benefit. The disease is associated with significant intra- and peritumoral inflammation and failure of protective immunosurveillance. Indeed, i...

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Autores principales: Steele, C W, Jamieson, N B, Evans, T R J, McKay, C J, Sansom, O J, Morton, J P, Carter, C R
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3619061/
https://www.ncbi.nlm.nih.gov/pubmed/23385734
http://dx.doi.org/10.1038/bjc.2013.24
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author Steele, C W
Jamieson, N B
Evans, T R J
McKay, C J
Sansom, O J
Morton, J P
Carter, C R
author_facet Steele, C W
Jamieson, N B
Evans, T R J
McKay, C J
Sansom, O J
Morton, J P
Carter, C R
author_sort Steele, C W
collection PubMed
description Pancreatic ductal adenocarcinoma (PDAC) is an aggressive malignancy associated with <5% 5-year survival, in which standard chemotherapeutics have limited benefit. The disease is associated with significant intra- and peritumoral inflammation and failure of protective immunosurveillance. Indeed, inflammatory signals are implicated in both tumour initiation and tumour progression. The major pathways regulating PDAC-associated inflammation are now being explored. Activation of leukocytes, and upregulation of cytokine and chemokine signalling pathways, both have been shown to modulate PDAC progression. Therefore, targeting inflammatory pathways may be of benefit as part of a multi-target approach to PDAC therapy. This review explores the pathways known to modulate inflammation at different stages of tumour development, drawing conclusions on their potential as therapeutic targets in PDAC.
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spelling pubmed-36190612013-04-08 Exploiting inflammation for therapeutic gain in pancreatic cancer Steele, C W Jamieson, N B Evans, T R J McKay, C J Sansom, O J Morton, J P Carter, C R Br J Cancer Minireview Pancreatic ductal adenocarcinoma (PDAC) is an aggressive malignancy associated with <5% 5-year survival, in which standard chemotherapeutics have limited benefit. The disease is associated with significant intra- and peritumoral inflammation and failure of protective immunosurveillance. Indeed, inflammatory signals are implicated in both tumour initiation and tumour progression. The major pathways regulating PDAC-associated inflammation are now being explored. Activation of leukocytes, and upregulation of cytokine and chemokine signalling pathways, both have been shown to modulate PDAC progression. Therefore, targeting inflammatory pathways may be of benefit as part of a multi-target approach to PDAC therapy. This review explores the pathways known to modulate inflammation at different stages of tumour development, drawing conclusions on their potential as therapeutic targets in PDAC. Nature Publishing Group 2013-03-19 2013-02-05 /pmc/articles/PMC3619061/ /pubmed/23385734 http://dx.doi.org/10.1038/bjc.2013.24 Text en Copyright © 2013 Cancer Research UK http://creativecommons.org/licenses/by-nc-sa/3.0/ This work is licensed under the Creative Commons Attribution-NonCommercial-Share Alike 3.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-sa/3.0/
spellingShingle Minireview
Steele, C W
Jamieson, N B
Evans, T R J
McKay, C J
Sansom, O J
Morton, J P
Carter, C R
Exploiting inflammation for therapeutic gain in pancreatic cancer
title Exploiting inflammation for therapeutic gain in pancreatic cancer
title_full Exploiting inflammation for therapeutic gain in pancreatic cancer
title_fullStr Exploiting inflammation for therapeutic gain in pancreatic cancer
title_full_unstemmed Exploiting inflammation for therapeutic gain in pancreatic cancer
title_short Exploiting inflammation for therapeutic gain in pancreatic cancer
title_sort exploiting inflammation for therapeutic gain in pancreatic cancer
topic Minireview
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3619061/
https://www.ncbi.nlm.nih.gov/pubmed/23385734
http://dx.doi.org/10.1038/bjc.2013.24
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