Cargando…

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...

Descripción completa

Detalles Bibliográficos
Autores principales: Liu, Wenbin, Deng, Yang, Li, Zishuai, Chen, Yifan, Zhu, Xiaoqiong, Tan, Xiaojie, Cao, Guangwen
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8645856/
https://www.ncbi.nlm.nih.gov/pubmed/34880864
http://dx.doi.org/10.3389/fimmu.2021.768098
_version_ 1784610397496541184
author Liu, Wenbin
Deng, Yang
Li, Zishuai
Chen, Yifan
Zhu, Xiaoqiong
Tan, Xiaojie
Cao, Guangwen
author_facet Liu, Wenbin
Deng, Yang
Li, Zishuai
Chen, Yifan
Zhu, Xiaoqiong
Tan, Xiaojie
Cao, Guangwen
author_sort Liu, Wenbin
collection PubMed
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 Online
Article
Text
id pubmed-8645856
institution National Center for Biotechnology Information
language English
publishDate 2021
publisher Frontiers Media S.A.
record_format MEDLINE/PubMed
spelling pubmed-86458562021-12-07 Cancer Evo–Dev: A Theory of Inflammation-Induced Oncogenesis Liu, Wenbin Deng, Yang Li, Zishuai Chen, Yifan Zhu, Xiaoqiong Tan, Xiaojie Cao, Guangwen Front Immunol Immunology 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. Frontiers Media S.A. 2021-11-22 /pmc/articles/PMC8645856/ /pubmed/34880864 http://dx.doi.org/10.3389/fimmu.2021.768098 Text en Copyright © 2021 Liu, Deng, Li, Chen, Zhu, Tan and Cao https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Immunology
Liu, Wenbin
Deng, Yang
Li, Zishuai
Chen, Yifan
Zhu, Xiaoqiong
Tan, Xiaojie
Cao, Guangwen
Cancer Evo–Dev: A Theory of Inflammation-Induced Oncogenesis
title 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_short Cancer Evo–Dev: A Theory of Inflammation-Induced Oncogenesis
title_sort cancer evo–dev: a theory of inflammation-induced oncogenesis
topic Immunology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8645856/
https://www.ncbi.nlm.nih.gov/pubmed/34880864
http://dx.doi.org/10.3389/fimmu.2021.768098
work_keys_str_mv AT liuwenbin cancerevodevatheoryofinflammationinducedoncogenesis
AT dengyang cancerevodevatheoryofinflammationinducedoncogenesis
AT lizishuai cancerevodevatheoryofinflammationinducedoncogenesis
AT chenyifan cancerevodevatheoryofinflammationinducedoncogenesis
AT zhuxiaoqiong cancerevodevatheoryofinflammationinducedoncogenesis
AT tanxiaojie cancerevodevatheoryofinflammationinducedoncogenesis
AT caoguangwen cancerevodevatheoryofinflammationinducedoncogenesis