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Inflammation-Related Carcinogenesis: Lessons from Animal Models to Clinical Aspects
SIMPLE SUMMARY: In multicellular organisms, inflammation is the body’s most primitive and essential protective response against any external agent. Inflammation, however, not only causes various modern diseases such as cardiovascular disorders, neurological disorders, autoimmune diseases, metabolic...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7926701/ https://www.ncbi.nlm.nih.gov/pubmed/33671768 http://dx.doi.org/10.3390/cancers13040921 |
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author | Okada, Futoshi Izutsu, Runa Goto, Keisuke Osaki, Mitsuhiko |
author_facet | Okada, Futoshi Izutsu, Runa Goto, Keisuke Osaki, Mitsuhiko |
author_sort | Okada, Futoshi |
collection | PubMed |
description | SIMPLE SUMMARY: In multicellular organisms, inflammation is the body’s most primitive and essential protective response against any external agent. Inflammation, however, not only causes various modern diseases such as cardiovascular disorders, neurological disorders, autoimmune diseases, metabolic syndrome, infectious diseases, and cancer but also shortens the healthy life expectancy. This review focuses on the onset of carcinogenesis due to chronic inflammation caused by pathogen infections and inhalation/ingestion of foreign substances. This study summarizes animal models associated with inflammation-related carcinogenesis by organ. By determining factors common to inflammatory carcinogenesis models, we examined strategies for the prevention and treatment of inflammatory carcinogenesis in humans. ABSTRACT: Inflammation-related carcinogenesis has long been known as one of the carcinogenesis patterns in humans. Common carcinogenic factors are inflammation caused by infection with pathogens or the uptake of foreign substances from the environment into the body. Inflammation-related carcinogenesis as a cause for cancer-related death worldwide accounts for approximately 20%, and the incidence varies widely by continent, country, and even region of the country and can be affected by economic status or development. Many novel approaches are currently available concerning the development of animal models to elucidate inflammation-related carcinogenesis. By learning from the oldest to the latest animal models for each organ, we sought to uncover the essential common causes of inflammation-related carcinogenesis. This review confirmed that a common etiology of organ-specific animal models that mimic human inflammation-related carcinogenesis is prolonged exudation of inflammatory cells. Genotoxicity or epigenetic modifications by inflammatory cells resulted in gene mutations or altered gene expression, respectively. Inflammatory cytokines/growth factors released from inflammatory cells promote cell proliferation and repair tissue injury, and inflammation serves as a “carcinogenic niche”, because these fundamental biological events are common to all types of carcinogenesis, not just inflammation-related carcinogenesis. Since clinical strategies are needed to prevent carcinogenesis, we propose the therapeutic apheresis of inflammatory cells as a means of eliminating fundamental cause of inflammation-related carcinogenesis. |
format | Online Article Text |
id | pubmed-7926701 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-79267012021-03-04 Inflammation-Related Carcinogenesis: Lessons from Animal Models to Clinical Aspects Okada, Futoshi Izutsu, Runa Goto, Keisuke Osaki, Mitsuhiko Cancers (Basel) Review SIMPLE SUMMARY: In multicellular organisms, inflammation is the body’s most primitive and essential protective response against any external agent. Inflammation, however, not only causes various modern diseases such as cardiovascular disorders, neurological disorders, autoimmune diseases, metabolic syndrome, infectious diseases, and cancer but also shortens the healthy life expectancy. This review focuses on the onset of carcinogenesis due to chronic inflammation caused by pathogen infections and inhalation/ingestion of foreign substances. This study summarizes animal models associated with inflammation-related carcinogenesis by organ. By determining factors common to inflammatory carcinogenesis models, we examined strategies for the prevention and treatment of inflammatory carcinogenesis in humans. ABSTRACT: Inflammation-related carcinogenesis has long been known as one of the carcinogenesis patterns in humans. Common carcinogenic factors are inflammation caused by infection with pathogens or the uptake of foreign substances from the environment into the body. Inflammation-related carcinogenesis as a cause for cancer-related death worldwide accounts for approximately 20%, and the incidence varies widely by continent, country, and even region of the country and can be affected by economic status or development. Many novel approaches are currently available concerning the development of animal models to elucidate inflammation-related carcinogenesis. By learning from the oldest to the latest animal models for each organ, we sought to uncover the essential common causes of inflammation-related carcinogenesis. This review confirmed that a common etiology of organ-specific animal models that mimic human inflammation-related carcinogenesis is prolonged exudation of inflammatory cells. Genotoxicity or epigenetic modifications by inflammatory cells resulted in gene mutations or altered gene expression, respectively. Inflammatory cytokines/growth factors released from inflammatory cells promote cell proliferation and repair tissue injury, and inflammation serves as a “carcinogenic niche”, because these fundamental biological events are common to all types of carcinogenesis, not just inflammation-related carcinogenesis. Since clinical strategies are needed to prevent carcinogenesis, we propose the therapeutic apheresis of inflammatory cells as a means of eliminating fundamental cause of inflammation-related carcinogenesis. MDPI 2021-02-22 /pmc/articles/PMC7926701/ /pubmed/33671768 http://dx.doi.org/10.3390/cancers13040921 Text en © 2021 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/). |
spellingShingle | Review Okada, Futoshi Izutsu, Runa Goto, Keisuke Osaki, Mitsuhiko Inflammation-Related Carcinogenesis: Lessons from Animal Models to Clinical Aspects |
title | Inflammation-Related Carcinogenesis: Lessons from Animal Models to Clinical Aspects |
title_full | Inflammation-Related Carcinogenesis: Lessons from Animal Models to Clinical Aspects |
title_fullStr | Inflammation-Related Carcinogenesis: Lessons from Animal Models to Clinical Aspects |
title_full_unstemmed | Inflammation-Related Carcinogenesis: Lessons from Animal Models to Clinical Aspects |
title_short | Inflammation-Related Carcinogenesis: Lessons from Animal Models to Clinical Aspects |
title_sort | inflammation-related carcinogenesis: lessons from animal models to clinical aspects |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7926701/ https://www.ncbi.nlm.nih.gov/pubmed/33671768 http://dx.doi.org/10.3390/cancers13040921 |
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