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Iron, inflammation and invasion of cancer cells

Chronic inflammation is associated with the metastasis of tumor cells evolving from a benign tumor to disseminating cancer. Such a metastatic progression is fostered by the angiogenesis propelled by various mediators interacting at the site of tumor growth. Angiogenesis causes two major changes that...

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Autores principales: FISCHER-FODOR, EVA, MIKLASOVA, NATALIA, BERINDAN-NEAGOE, IOANA, SAHA, BHASKAR
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Iuliu Hatieganu University of Medicine and Pharmacy 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4632882/
https://www.ncbi.nlm.nih.gov/pubmed/26609256
http://dx.doi.org/10.15386/cjmed-492
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author FISCHER-FODOR, EVA
MIKLASOVA, NATALIA
BERINDAN-NEAGOE, IOANA
SAHA, BHASKAR
author_facet FISCHER-FODOR, EVA
MIKLASOVA, NATALIA
BERINDAN-NEAGOE, IOANA
SAHA, BHASKAR
author_sort FISCHER-FODOR, EVA
collection PubMed
description Chronic inflammation is associated with the metastasis of tumor cells evolving from a benign tumor to disseminating cancer. Such a metastatic progression is fostered by the angiogenesis propelled by various mediators interacting at the site of tumor growth. Angiogenesis causes two major changes that are assisted by altered glycosylation and neo-antigen presentation by the cancer cells. The angiogenesis-promoted pathological changes include enhanced inflammation and degradation of tissue matrices releasing tumor cells from the site of its origin. The degraded tumor cells release the neo-antigens resulting from altered glycosylation. Presentation of neo-antigens to T cells escalates metastasis and inflammation. Inflammasome activation and inflammation in several infections are regulated by iron. Based on the discrete reports, we propose a link between iron, inflammation, angiogenesis and tumor growth. Knowing the link better may help us formulate a novel strategy for cancer immunotherapy.
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spelling pubmed-46328822015-11-25 Iron, inflammation and invasion of cancer cells FISCHER-FODOR, EVA MIKLASOVA, NATALIA BERINDAN-NEAGOE, IOANA SAHA, BHASKAR Clujul Med Review Chronic inflammation is associated with the metastasis of tumor cells evolving from a benign tumor to disseminating cancer. Such a metastatic progression is fostered by the angiogenesis propelled by various mediators interacting at the site of tumor growth. Angiogenesis causes two major changes that are assisted by altered glycosylation and neo-antigen presentation by the cancer cells. The angiogenesis-promoted pathological changes include enhanced inflammation and degradation of tissue matrices releasing tumor cells from the site of its origin. The degraded tumor cells release the neo-antigens resulting from altered glycosylation. Presentation of neo-antigens to T cells escalates metastasis and inflammation. Inflammasome activation and inflammation in several infections are regulated by iron. Based on the discrete reports, we propose a link between iron, inflammation, angiogenesis and tumor growth. Knowing the link better may help us formulate a novel strategy for cancer immunotherapy. Iuliu Hatieganu University of Medicine and Pharmacy 2015 2015-07-01 /pmc/articles/PMC4632882/ /pubmed/26609256 http://dx.doi.org/10.15386/cjmed-492 Text en This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License (http://creativecommons.org/licenses/by-nc-nd/4.0/)
spellingShingle Review
FISCHER-FODOR, EVA
MIKLASOVA, NATALIA
BERINDAN-NEAGOE, IOANA
SAHA, BHASKAR
Iron, inflammation and invasion of cancer cells
title Iron, inflammation and invasion of cancer cells
title_full Iron, inflammation and invasion of cancer cells
title_fullStr Iron, inflammation and invasion of cancer cells
title_full_unstemmed Iron, inflammation and invasion of cancer cells
title_short Iron, inflammation and invasion of cancer cells
title_sort iron, inflammation and invasion of cancer cells
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4632882/
https://www.ncbi.nlm.nih.gov/pubmed/26609256
http://dx.doi.org/10.15386/cjmed-492
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