Cancer Evo-Dev, a novel hypothesis derived from studies on hepatitis B virus-induced carcinogenesis

Cao, Guangwen

doi:10.20517/2394-5079.2017.45

Cited by 10 publications

(9 citation statements)

References 132 publications

(177 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Among anti-HBe carriers with advanced CLD, targeting the much lower levels of ccc DNA may not be effective in preventing progression to cirrhosis and HCC, because at this stage, most of the HBx made probably comes from integrated templates. Under these circumstances, ccc DNA may persist in a transcriptionally inactive form, which is consistent with the absence of HBV DNA in the blood, even after treatment with direct acting anti-viral agents or therapy aimed at stimulating immune responses against virus infected cells [101,102]. In fact, early work already pointed out that seroconversion to anti-HBe is sometimes associated with the progression of CLD [103,104], even though later work showed that disease progression was associated with continued replication of HBV DNA carrying one or more mutations in the core gene that blocks production of HBeAg [27].…”

Section: Hbx and Inflammationmentioning

confidence: 78%

Pathogenesis of Hepatitis B Virus Associated Chronic Liver Disease

Feitelson¹

2018

Liver Cancer

View full text Add to dashboard Cite

Hepatitis B virus (HBV) infection is associated with chronic liver diseases (CLD), which progress from hepatitis to fibrosis, cirrhosis, and finally hepatocellular carcinoma (HCC) over 30-50 years. The pathogenesis of CLD is immune mediated, which is characterized by persistent immune responses against virus infected hepatocytes. During bouts of CLD, the virus gene encoding the hepatitis B x antigen (HBx) is increasingly found integrated at multiple sites within the human genome. Many of these integrated templates express HBx, which is a trans-regulatory protein that supports virus gene expression and replication on one hand, but also alters patterns of gene expression in the infected cell. HBx alters gene expression by constitutively activating signal transduction pathways in the cytoplasm and promoting epigenetic mediated changes in the expression of cellular genes. In doing so, HBx contributes to the persistence of virus infected cells and to the pathogenesis of CLD by triggering multiple hallmarks which are characteristic of cancer.

show abstract

Section: Hbx and Inflammationmentioning

confidence: 78%

Pathogenesis of Hepatitis B Virus Associated Chronic Liver Disease

Feitelson¹

2018

Liver Cancer

View full text Add to dashboard Cite

show abstract

“…By summarizing evidence from a variety of perspectives, we gradually proposed and modified the theory of Cancer Evo-Dev (12). The framework of this theory is as follows (Figure 1):…”

Section: The Framework and Rationale Of Cancer Evo-devmentioning

confidence: 99%

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

Liu

Deng

et al. 2021

Front. Immunol.

View full text Add to dashboard Cite

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.

show abstract

“…The integration of evolution and developmental biology was termed Evo-Devo [12,13]. In this chapter, we present a scientific theory of Cancer Evolution-Development (Cancer Evo-Dev) based on the current understanding of HBV-HCC [14]. This theoretical hypothesis can provide an evolutionary insight of profiling HCC risk and developing more reasonable predictive and prognostic strategies.…”

Section: Introductionmentioning

confidence: 99%

Hepatitis B Virus (HBV) - Induced Hepatocarcinogenesis, a Founding Framework of Cancer Evolution and Development (Cancer Evo-Dev)

Liu¹,

Cao²

2022

Hepatocellular Carcinoma - Challenges and Opportunities of a Multidisciplinary Approach

View full text Add to dashboard Cite

In this chapter, we present the founding framework of a novel theory termed as Cancer Evolution-Development (Cancer Evo-Dev), based on the current understanding of hepatitis B virus (HBV) induced hepatocarcinogenesis. The interactions of genetic predispositions and HBV infection is responsible for the maintenance of chronic non-resolving inflammation. Under the inflammatory microenvironment, pro-inflammatory factors trans-activate the expression of cytidine deaminases and suppress the expression of uracil DNA glycosylase. The imbalance between the mutagenic forces and mutation-correcting forces facilitates the generations of somatic mutations, viral mutations, and viral integrations into the host genomes. The majority of cells with genomic mutations and mutated viruses are eliminated in survival competition. Only a small percentage of the mutated cells adapted to the hostile environment can survive, retro-differentiate, and function as cancer-initiating cells, representing a process of “mutation-selection-adaptation”. Cancer Evo-Dev lays the theoretical foundation for understanding the mechanisms by which chronic infection of HBV promotes hepatocarcinogenesis. This theory also plays an important role in specific prophylaxis, prediction, early diagnosis, and targeted treatment of cancers.

show abstract

Cancer Evo-Dev, a novel hypothesis derived from studies on hepatitis B virus-induced carcinogenesis

Cited by 10 publications

References 132 publications

Pathogenesis of Hepatitis B Virus Associated Chronic Liver Disease

Pathogenesis of Hepatitis B Virus Associated Chronic Liver Disease

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

Hepatitis B Virus (HBV) - Induced Hepatocarcinogenesis, a Founding Framework of Cancer Evolution and Development (Cancer Evo-Dev)

Contact Info

Product

Resources

About