The role of APOBEC3B in the development of hepatocellular carcinoma should be investigated with the consideration of hepatitis B virus evolution

Liu, Wenbin; Cao, Guangwen

doi:10.20517/2394-5079.2019.27

Cited by 1 publication

(1 citation statement)

References 11 publications

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“…HCC-related HBV mutations are selected by the immune microenvironment before the occurrence of HCC. The deficiency of CD8 + T cell epitopes is one of the main features of HBV mutations, which facilitates evading immune eradication (87,88). HBV mutations posing a significant HCC risk are located mainly within the Enhancer II (EnhII)/basal core promoter (BCP)/precore region and preS regions (89)(90)(91)(92).…”

Section: Evolutionmentioning

confidence: 99%

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

Liu

Deng

et al. 2021

Front. Immunol.

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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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