Hepatitis B Virus Combo Mutations Improve the Prediction and Active Prophylaxis of Hepatocellular Carcinoma: A Clinic-Based Cohort Study

Yin, Jianhua; Wang, Junxue; Pu, Rui; Xin, Haiguang; Li, Zixiong; Han, Xue; Ding, Yibo; Du, Yan; Liu, Wenbin; Deng, Yang; Wu, Ming; Yu, Ming; Zhang, Hongwei; Wang, Hongyang; Thompson, Timothy C.; Ni, Wei; Cao, Guangwen

doi:10.1158/1940-6207.capr-15-0160

Cited by 25 publications

(42 citation statements)

References 38 publications

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“…Thirdly, due to lack of data, our analyses did not adjust for HBV genotype and HBV mutations. Both HBV genotype and HBV mutation in the precore/enhancer II region and the preS region have been reported to be independent HCC risk factors in CHB patients162728293031. It is not clear whether persistence of elevated serum TBA is associated with specific HBV genotypes or specific HBV variants in our cohort.…”

Section: Discussionmentioning

confidence: 81%

Increased hepatocellular carcinoma risk in chronic hepatitis B patients with persistently elevated serum total bile acid: a retrospective cohort study

Wang

Shang

Wan

et al. 2016

Sci Rep

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To investigate the association between long-term changes of serum total bile acid and hepatocellular carcinoma in chronic hepatitis B patients, we did a retrospective cohort study of 2262 chronic hepatitis B patients with regular antiviral treatment using data from the Hepatitis Biobank at Southwest Hospital Program from 2004 to 2014. Patients in the study were classified into 3 groups according to persistence of elevated serum total bile acid during follow-up: none-low, medium, and high persistence of elevated serum total bile acid. The association between persistence of elevated serum total bile acid and hepatocellular carcinoma was estimated using Cox proportional hazard models and Kaplan-Meier analysis including information about patients’ demographic and clinical characteristics. There were 62 hepatocellular carcinoma cases during a total follow-up of 14756.5 person-years in the retrospective study. Compared to patients with none-low persistence of elevated total bile acid, the multivariate adjusted hazard ratios (95% confidence interval) were 2.37 (1.16–4.84), and 2.57 (1.28–5.16) for patients with medium, and high persistence of elevated total bile acid. Our findings identified persistence of elevated serum total bile acid as an independent risk factor of hepatocellular carcinoma in chronic hepatitis B patients.

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Section: Discussionmentioning

confidence: 81%

Increased hepatocellular carcinoma risk in chronic hepatitis B patients with persistently elevated serum total bile acid: a retrospective cohort study

Wang

Shang

Wan

et al. 2016

Sci Rep

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“…Expanding worldwide access to HBV vaccination is a harbinger of benefits to come. Recent work suggests that specific HBV mutations can predict antiviral preventive efficacy bringing precision medicine into this field (49). Global perspectives on the patterns of HPV-related cancers (e.g., oropharyngeal) and preventing virally related cancers with vaccines, including efforts to make these vaccines available to countries experiencing financial hardships, highlight the burden and challenges of these viral diseases (50, 51).…”

Section: Immunopreventionmentioning

confidence: 99%

Transforming Cancer Prevention through Precision Medicine and Immune-oncology

Kensler

Spira

Garber

et al. 2016

Cancer Prevention Research

136

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We have entered a transformative period in the history of cancer prevention. Recent remarkable advances in sequencing technology and computational biology have now provided us with unprecedented opportunities to study the biology of premalignancy, including deep genomic characterization of these lesions, and a detailed assessment of the tumor immune microenvironment. This extraordinary technology has enabled development of novel genomic biomarkers to personalize cancer detection, identified driver mutations in circulating DNA from patients with premalignant lesions, and defined immune gene signatures that are predictive of progression to invasive malignancy. More recently, we have witnessed the remarkable realization of the early promise of immunotherapy which has emanated from a deep understanding of the complexities of the immune system. Just as precision therapy and immunotherapy are transforming cancer treatment, precision medicine and immunoprevention approaches are being translated to the clinic and showing great promise. Here, we set out a brief agenda for the immediate future of cancer prevention, which will involve precision medicine and immunoprevention – pivotal elements of a broader domain of personalized public health.

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“…The so-called "dose-dependently" is referred to that the HCC risk is significantly higher in the CHB patients carrying one of the three mutations than in those without the mutation, is significantly higher in those with two of the three mutation than in those with one of the three mutation, and is also significantly higher in those with all the three mutation than in those with two of the three mutations. Thus, the baseline HBV mutations in combination are able to predict the occurrence of HCC in CHB patients [33] . Several longitudinal studies carried in China have also demonstrated that baseline A1762T/G1764A mutation increases the risk of HCC in chronic HBV carriers or CHB patients [34][35][36][37] .…”

Section: "Dead-end" Evolution Of Hbvmentioning

confidence: 99%

“…The HCC-related HBV mutated X or large S fragments promote the malignant phenotypes As described above, the baseline HBV mutations including A1762T/G1764A, C1653T, and T1753Vin the 3' terminal of HBx gene in sera "dose-dependently" predict the occurrence of HCC in longitudinal studies, especially cohort studies [33][34][35][36][37] . The frequency of HBV preS deletion also increases consecutively from ASCs to HCC and preS mutation is associated with a 3.77-fold increased risk of HCC [32] .…”

Section: Reduction Of Cd8mentioning

confidence: 99%

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

Cao¹

2017

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How to cite this article: Cao GW. Cancer Evo-Dev, a novel hypothesis derived from studies on hepatitis B virus-induced carcinogenesis. Hepatoma Res 2017;3:241-59.Non-resolving inflammation, which may be maintained by infection, pollution, and metabolic stimulants and their interactions with immunogenetic predisposition, provides a fertile field for cancer development. This is strongly evident in hepatocellular carcinoma. Here, the framework of a hypothesis called Cancer Evo-Dev is presented, based on the advances in hepatitis B virusinduced hepatocarcinogenesis. Several aspects central to this theory are as follows: (1) immune imbalance caused by the interaction of immunogenetic predispositions and hepatitis B virus infection maintains non-resolving inflammation; (2) active inflammation executants promote mutations in viral and host genomes via disbalancing mutagenic forces including cytidine deaminases and mutation-repairing forces including uracil-DNA glycosylases, thus promoting cancer-related somatic mutations and viral mutations; (3) a small percentage of the cells whose somatic mutations alter the survival signalling adapt to the inflammatory microenvironment, de-differentiate via demethylating role of cytidine deaminases, and reversely develop into tumor-initiating cells (TICs); (4) under the cultivation of some factors like POSTN from tumorinfiltrating fibroblasts and M2 macrophages, TICs acquire the stemness, cancer-stem cells obtain distinct metastatic and drug-resistant potentials under the selection pressure from distinct microenvironments; (5) glycolysis persistence in the presence of oxygen provides essential energy for cell survival and the raw material for DNA synthesis. Thus, cancer development is characterized by an evolutionary process of "mutation-selection-adaptation". The framework of Cancer Evo-Dev can be verified in other cancers. Cancer Evo-Dev lays theoretical foundation for understanding the mechanisms by which inflammation promotes cancer development, and it also plays a role in specific prophylaxis, prediction, and targeted treatment of cancers. Key words:Inflammation, hepatitis B virus, mutations, hepatoma, Cancer Evo-Dev ABSTRACTArticle history:

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Hepatitis B Virus Combo Mutations Improve the Prediction and Active Prophylaxis of Hepatocellular Carcinoma: A Clinic-Based Cohort Study

Cited by 25 publications

References 38 publications

Increased hepatocellular carcinoma risk in chronic hepatitis B patients with persistently elevated serum total bile acid: a retrospective cohort study

Increased hepatocellular carcinoma risk in chronic hepatitis B patients with persistently elevated serum total bile acid: a retrospective cohort study

Transforming Cancer Prevention through Precision Medicine and Immune-oncology

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

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