Cancer Evo-Dev: A Theory of Inflammation-Induced Oncogenesis.
Cancer Evo-Dev: A Theory of Inflammation-Induced Oncogenesis.
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DOI：
10.3389/fimmu.2021.768098
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发表时间：
2021
影响因子：
7.3
通讯作者：
Cao G
中科院分区：
文献类型：
--
作者：
Liu W;Deng Y;Li Z;Chen Y;Zhu X;Tan X;Cao G
慢性炎症是癌症发展的先决条件。在这里，我们提出了一个新的理论框架，称为癌症进化发展（癌症Evo-Dev）的基础上，目前的理解炎症相关的致癌作用，特别是慢性感染B型肝炎病毒引起的肝癌。遗传易感性和环境暴露（如病毒感染）之间的相互作用维持了慢性非消退性炎症。污染、代谢综合征、缺乏身体活动、衰老和不良的社会心理暴露也会通过诱发慢性低度阴燃性炎症增加患癌症的风险。在炎症未消退的微环境下，促炎因子通过诱导胞苷脱氨酶等致突变力与尿嘧啶-DNA糖基化酶等突变校正力之间的失衡，促进体细胞突变和病毒突变的产生。大多数具有体细胞突变和突变病毒的细胞在生存竞争中被淘汰。只有一小部分突变细胞存活下来，适应恶劣的环境，逆分化，并通过改变信号通路作为癌症起始细胞发挥作用。这些引发癌症的细胞获得干细胞，重新编程代谢模式，并影响微环境。致癌过程遵循“突变-选择-适应”的规律。慢性体力活动通过上调NK细胞和淋巴细胞的活性和数量以及延长白细胞端粒来降低炎症水平;下调促炎细胞因子包括白细胞介素-6和衰老淋巴细胞，特别是在老年人群中。抗炎药物可以减少癌症的发生和复发。靶向癌症干性信号通路可能导致癌症根除。癌症Evo-Dev不仅有助于了解炎症促进癌症发展的机制，还为各种癌症的有效预防和靶向治疗奠定了基础。
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.
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影响因子：
7.3
作者：
Ferriere A;Santa P;Garreau A;Bandopadhyay P;Blanco P;Ganguly D;Sisirak V
通讯作者：
Sisirak V
色氨酸衍生物调节干细胞样癌细胞中 Oct4 的转录。
影响因子：
16.6
作者：
Cheng, Jie;Li, Wenxin;Kang, Bo;Zhou, Yanwen;Song, Jiasheng;Dan, Songsong;Yang, Ying;Zhang, Xiaoqian;Li, Jingchao;Yin, Shengyong;Cao, Hongcui;Yao, Hangping;Zhu, Chenggang;Yi, Wen;Zhao, Qingwei;Xu, Xiaowei;Zheng, Min;Zheng, Shusen;Li, Lanjuan;Shen, Binghui;Wang, Ying-Jie
通讯作者：
Wang, Ying-Jie
影响因子：
2.5
作者：
Deng, Yang;Li, Peng;Cao, Guangwen
通讯作者：
Cao, Guangwen
影响因子：
11.2
作者：
Ahn, Eun Hyun;Lee, Seung Hyuk;Loeb, Lawrence A.
通讯作者：
Loeb, Lawrence A.
DOI：
10.1126/science.1253462
发表时间：
2014-10-10
期刊：
Science (New York, N.Y.)
影响因子：
--
作者：
de Bruin EC;McGranahan N;Mitter R;Salm M;Wedge DC;Yates L;Jamal-Hanjani M;Shafi S;Murugaesu N;Rowan AJ;Grönroos E;Muhammad MA;Horswell S;Gerlinger M;Varela I;Jones D;Marshall J;Voet T;Van Loo P;Rassl DM;Rintoul RC;Janes SM;Lee SM;Forster M;Ahmad T;Lawrence D;Falzon M;Capitanio A;Harkins TT;Lee CC;Tom W;Teefe E;Chen SC;Begum S;Rabinowitz A;Phillimore B;Spencer-Dene B;Stamp G;Szallasi Z;Matthews N;Stewart A;Campbell P;Swanton C
通讯作者：
Swanton C