Cancer Evo–Dev: A Theory of Inflammation-Induced Oncogenesis

Chronic inflammation is a prerequisite for the development of cancers. Here, we present the framework of a novel theory termed as Cancer Evolution-Development (Cancer Evo-Dev) based on the current understanding of inflammation-related carcinogenesis, especially hepatocarcinogenesis induced by chroni...

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Autores principales:	Wenbin Liu, Yang Deng, Zishuai Li, Yifan Chen, Xiaoqiong Zhu, Xiaojie Tan, Guangwen Cao
Formato:	article
Lenguaje:	EN
Publicado:	Frontiers Media S.A. 2021
Materias:	cancer evolution inflammation mutation viral infection Immunologic diseases. Allergy RC581-607
Acceso en línea:	https://doaj.org/article/53cf43a0100448aab16ee3bc5d8335a7
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spelling	oai:doaj.org-article:53cf43a0100448aab16ee3bc5d8335a72021-11-22T06:25:06ZCancer Evo–Dev: A Theory of Inflammation-Induced Oncogenesis1664-322410.3389/fimmu.2021.768098https://doaj.org/article/53cf43a0100448aab16ee3bc5d8335a72021-11-01T00:00:00Zhttps://www.frontiersin.org/articles/10.3389/fimmu.2021.768098/fullhttps://doaj.org/toc/1664-3224Chronic inflammation is a prerequisite for the development of cancers. Here, we present the framework of a novel theory termed as Cancer Evolution-Development (Cancer Evo-Dev) based on the current understanding of inflammation-related carcinogenesis, especially hepatocarcinogenesis induced by chronic infection with hepatitis B virus. The interaction between genetic predispositions and environmental exposures, such as viral infection, maintains chronic non-resolving inflammation. Pollution, metabolic syndrome, physical inactivity, ageing, and adverse psychosocial exposure also increase the risk of cancer via inducing chronic low-grade smoldering inflammation. Under the microenvironment of non-resolving inflammation, pro-inflammatory factors facilitate the generation of somatic mutations and viral mutations by inducing the imbalance between the mutagenic forces such as cytidine deaminases and mutation-correcting forces including uracil–DNA glycosylase. Most cells with somatic mutations and mutated viruses are eliminated in survival competition. Only a small percentage of mutated cells survive, adapt to the hostile environment, retro-differentiate, and function as cancer-initiating cells via altering signaling pathways. These cancer-initiating cells acquire stem-ness, reprogram metabolic patterns, and affect the microenvironment. The carcinogenic process follows the law of “mutation-selection-adaptation”. Chronic physical activity reduces the levels of inflammation via upregulating the activity and numbers of NK cells and lymphocytes and lengthening leukocyte telomere; downregulating proinflammatory cytokines including interleukin-6 and senescent lymphocytes especially in aged population. Anti-inflammation medication reduces the occurrence and recurrence of cancers. Targeting cancer stemness signaling pathways might lead to cancer eradication. Cancer Evo-Dev not only helps understand the mechanisms by which inflammation promotes the development of cancers, but also lays the foundation for effective prophylaxis and targeted therapy of various cancers.Wenbin LiuYang DengZishuai LiYifan ChenXiaoqiong ZhuXiaojie TanGuangwen CaoFrontiers Media S.A.articlecancerevolutioninflammationmutationviral infectionImmunologic diseases. AllergyRC581-607ENFrontiers in Immunology, Vol 12 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	cancer evolution inflammation mutation viral infection Immunologic diseases. Allergy RC581-607
spellingShingle	cancer evolution inflammation mutation viral infection Immunologic diseases. Allergy RC581-607 Wenbin Liu Yang Deng Zishuai Li Yifan Chen Xiaoqiong Zhu Xiaojie Tan Guangwen Cao Cancer Evo–Dev: A Theory of Inflammation-Induced Oncogenesis
description	Chronic inflammation is a prerequisite for the development of cancers. Here, we present the framework of a novel theory termed as Cancer Evolution-Development (Cancer Evo-Dev) based on the current understanding of inflammation-related carcinogenesis, especially hepatocarcinogenesis induced by chronic infection with hepatitis B virus. The interaction between genetic predispositions and environmental exposures, such as viral infection, maintains chronic non-resolving inflammation. Pollution, metabolic syndrome, physical inactivity, ageing, and adverse psychosocial exposure also increase the risk of cancer via inducing chronic low-grade smoldering inflammation. Under the microenvironment of non-resolving inflammation, pro-inflammatory factors facilitate the generation of somatic mutations and viral mutations by inducing the imbalance between the mutagenic forces such as cytidine deaminases and mutation-correcting forces including uracil–DNA glycosylase. Most cells with somatic mutations and mutated viruses are eliminated in survival competition. Only a small percentage of mutated cells survive, adapt to the hostile environment, retro-differentiate, and function as cancer-initiating cells via altering signaling pathways. These cancer-initiating cells acquire stem-ness, reprogram metabolic patterns, and affect the microenvironment. The carcinogenic process follows the law of “mutation-selection-adaptation”. Chronic physical activity reduces the levels of inflammation via upregulating the activity and numbers of NK cells and lymphocytes and lengthening leukocyte telomere; downregulating proinflammatory cytokines including interleukin-6 and senescent lymphocytes especially in aged population. Anti-inflammation medication reduces the occurrence and recurrence of cancers. Targeting cancer stemness signaling pathways might lead to cancer eradication. Cancer Evo-Dev not only helps understand the mechanisms by which inflammation promotes the development of cancers, but also lays the foundation for effective prophylaxis and targeted therapy of various cancers.
format	article
author	Wenbin Liu Yang Deng Zishuai Li Yifan Chen Xiaoqiong Zhu Xiaojie Tan Guangwen Cao
author_facet	Wenbin Liu Yang Deng Zishuai Li Yifan Chen Xiaoqiong Zhu Xiaojie Tan Guangwen Cao
author_sort	Wenbin Liu
title	Cancer Evo–Dev: A Theory of Inflammation-Induced Oncogenesis
title_short	Cancer Evo–Dev: A Theory of Inflammation-Induced Oncogenesis
title_full	Cancer Evo–Dev: A Theory of Inflammation-Induced Oncogenesis
title_fullStr	Cancer Evo–Dev: A Theory of Inflammation-Induced Oncogenesis
title_full_unstemmed	Cancer Evo–Dev: A Theory of Inflammation-Induced Oncogenesis
title_sort	cancer evo–dev: a theory of inflammation-induced oncogenesis
publisher	Frontiers Media S.A.
publishDate	2021
url	https://doaj.org/article/53cf43a0100448aab16ee3bc5d8335a7
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Cancer Evo–Dev: A Theory of Inflammation-Induced Oncogenesis

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