Antiviral Therapy Inhibits Viral Reactivation and Improves Survival after Repeat Hepatectomy for Hepatitis B Virus-Related Recurrent Hepatocellular Carcinoma

Huang, Shengyu; Xia, Yong; Lei, Zhengqing; Zou, Qifei; Li, Jun; Yang, Tian; Wang, Kui; Yan, Zhenlin; Wan, Xia

doi:10.1016/j.jamcollsurg.2016.11.009

Cited by 25 publications

(39 citation statements)

References 40 publications

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“…39 Additionally, several epidemiological investigations suggested that antiviral treatment could improve the survival and decrease the recurrence of HBV-related HCC. 40 Taken together, serum HBV level might be utilized for patients' immunity response evaluation, while combine therapy with antiviral drugs in antitumor treatment could greatly benefit for T cell activation in HBV-related HCC patients.…”

Section: Clinical Correlation Between Il12-mediated Pathway and Hcc Pmentioning

confidence: 99%

Genomic and transcriptional Profiling of tumor infiltrated CD8⁺ T cells revealed functional heterogeneity of antitumor immunity in hepatocellular carcinoma

Chen

Cai

et al. 2018

OncoImmunology

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As key players in HCC antitumor response, the functions of tumor infiltrated CD8 + T cells are significantly affected by surrounding microenvironment. A detailed profiling of their genomic and transcriptional changes could provide valuable insights for both future immunotherapy development and prognosis evaluation. We performed whole exome and transcriptome sequencing on tumor infiltrated CD8 + T cells and CD8 + T cells isolated from other tissue origins (peritumor tissues and corresponding PBMCs) in eight treatment-naive HCC patients. The results demonstrated that transcriptional changes, rather than genomic alterations were the main contributors to the functional alterations of CD8 + T cells in the process of tumor progression. The origins of CD8 + T cells defined their transcriptional landscape, while the tumor infiltrated CD8 + T cells shared more similarity with peritumor-derived CD8 + T cells compared with those CD8 + T cells in blood. In addition, tumor infiltrated CD8 + T cells also showed larger transcriptional heterogeneity among individuals, which was modulated by clinical features such as HBV levels, preoperative anti-viral treatment and the degree of T cell infiltration. We also identified multiple interconnected pathways involved in the activation and exhaustion of tumor infiltrated CD8 + T cells, among which IL-12 mediated pathway could dynamically reflect the functional status of CD8 + TILs and activation of this pathway indicated a better prognosis. Our results presented an overview picture of CD8 + TILs' genomic and transcriptional landscape and features, as well as how the functional status of CD8 + TILs correlated with patients' clinical course.

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Section: Clinical Correlation Between Il12-mediated Pathway and Hcc Pmentioning

confidence: 99%

Genomic and transcriptional Profiling of tumor infiltrated CD8⁺ T cells revealed functional heterogeneity of antitumor immunity in hepatocellular carcinoma

Chen

Cai

et al. 2018

OncoImmunology

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“…For those with HCC recurrence, a preserved liver function at the time of recurrence via the use of antiviral therapy increased the proportion of patients that can receive curative treatment [63,64] . For patients with repeat hepatectomy for recurrent HCC, antiviral therapy was also associated with better long-term prognosis [65] .…”

Section: Antiviral Therapy For Hcc Patients Undergoing Surgical Resecmentioning

confidence: 99%

The role of oral antiviral therapy in hepatitis B-related hepatocellular carcinoma

Fung¹,

Chok²

2017

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Hepatitis B virus (HBV) is the leading cause of hepatocellular carcinoma (HCC) in places where chronic hepatitis B infection is endemic. Oral nucleos(t)ide analog (NA) therapy can reduce the risk of HCC, but cannot completely prevent its development. For HBV-related HCCs, viral inhibition by NAs can preserve or improve liver function, thereby increasing the chance of therapeutic intervention. After surgical resection, NAs can prevent reactivation of HBV, and also reduce the chance of de novo development of HCC in the remnant liver. For those who undergo liver transplantation, NAs are essential to prevent reactivation and graft hepatitis, but is not likely to prevent HCC recurrence, which is due to metastatic disease. The role of NAs for non-curable advanced HCC is less well defined. These include patients undergoing locoregional therapy, chemotherapy, or palliation. Although antiviral therapy can preserve liver function, which may be compromised by HBV, it is unable to prevent disease progression from HCC. At the time of HCC diagnosis, most patients will already be receiving NAs, and these patients should be maintained on therapy. For patients not on antiviral therapy at the time of HCC diagnosis, the decision to commence therapy is often determined by the stage of HCC and life expectancy. Patients undergoing curative therapy, or locoregional therapy/chemotherapy with reasonable life expectancy, should be commenced on antiviral therapy. Key words:Antiviral therapy, hepatitis B virus, hepatocellular carcinoma ABSTRACTArticle history:

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“…This indicates that HBV evolution in adjacent tissues continues until the patient dies. Antiviral therapy that can attenuate viral replication and subsequent hepatic inflammation notably promotes postoperative prognosis of HBV-HCC patients [50][51][52][53] , possibly because antiviral treatment can block HBV evolution in adjacent hepatic tissues and also likely in remaining HCC tissues.…”

Section: Reduction Of Cd8mentioning

confidence: 99%

“…The synergistic effect of those three cytokines can promote the transformation of normal hepatocytes into stem-like cells. Antiviral therapy can significantly reduce the risks of occurrence and postoperative recurrence by HCC via relieving hepatic inflammation [50][51][52][53]119] , possibly because termination of inflammation can destroy the fertile environment for cancer evolution.…”

Section: Apobecs Bridge Inflammation and Cancermentioning

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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Antiviral Therapy Inhibits Viral Reactivation and Improves Survival after Repeat Hepatectomy for Hepatitis B Virus-Related Recurrent Hepatocellular Carcinoma

Cited by 25 publications

References 40 publications

Genomic and transcriptional Profiling of tumor infiltrated CD8⁺ T cells revealed functional heterogeneity of antitumor immunity in hepatocellular carcinoma

Genomic and transcriptional Profiling of tumor infiltrated CD8⁺ T cells revealed functional heterogeneity of antitumor immunity in hepatocellular carcinoma

The role of oral antiviral therapy in hepatitis B-related hepatocellular carcinoma

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

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Antiviral Therapy Inhibits Viral Reactivation and Improves Survival after Repeat Hepatectomy for Hepatitis B Virus-Related Recurrent Hepatocellular Carcinoma

Cited by 25 publications

References 40 publications

Genomic and transcriptional Profiling of tumor infiltrated CD8+ T cells revealed functional heterogeneity of antitumor immunity in hepatocellular carcinoma

Genomic and transcriptional Profiling of tumor infiltrated CD8+ T cells revealed functional heterogeneity of antitumor immunity in hepatocellular carcinoma

The role of oral antiviral therapy in hepatitis B-related hepatocellular carcinoma

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

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Product

Resources

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Genomic and transcriptional Profiling of tumor infiltrated CD8⁺ T cells revealed functional heterogeneity of antitumor immunity in hepatocellular carcinoma

Genomic and transcriptional Profiling of tumor infiltrated CD8⁺ T cells revealed functional heterogeneity of antitumor immunity in hepatocellular carcinoma