What Comes First: Treatment of Viral Hepatitis or Liver Cancer?

Feld, Jordan J.; Krassenburg, Lisette

doi:10.1007/s10620-019-05518-5

Cited by 12 publications

(10 citation statements)

References 45 publications

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“…[74][75][76] It was later determined that patients who received DAA tended to be older and had more advanced disease or comorbidities compared to the untreated or IF-treated individuals in the comparison groups. 77 The adjusted estimates in our study reduced these biases and showed that DAAs are not associated with increased hazard of HCC recurrence (aHR: 0.70; 95% CI: 0.42-1.15), and in fact may reduce the hazard of HCC occurrence (aHR: 0.67; 95% CI: 0.54-0.84). Similarly, to account for patient differences, Waziry et al conducted a meta-regression and showed no evidence for an increased risk of HCC occurrence or recurrence following SVR after treatment with DAAs vs IF-based regimens (RR = 0.67; 95% CI: 0.16-2.77 for de novo HCC, and RR = 0.62; 95% CI: 0.11-3.45 for HCC recurrence).…”

Section: Discussionmentioning

confidence: 49%

Impact of direct‐acting antiviral regimens on mortality and morbidity outcomes in patients with chronic hepatitis c: Systematic review and meta‐analysis

Sahakyan

Lee-Kim

Bremner

et al. 2021

Journal of Viral Hepatitis

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Over seventy million people worldwide suffer from chronic hepatitis C (CHC), which can lead to liver failure and hepatocellular carcinoma (HCC). 1 Worldwide, an estimated 400,000 deaths per year can be attributed to liver disease caused by hepatitis C virus (HCV). 1 Until recently, interferon (IF)-based drug regimens were the mainstay of treatment for HCV. 2 However, most of these drugs caused side effects, required up to 48 weeks of therapy and had relatively low sustained virologic response (SVR) rates, a welldocumented surrogate indicator for HCV cure. 2 The introduction of direct-acting antivirals (DAAs) in 2011 revolutionized treatment for HCV. DAAs quickly became the recommended first-line treatment

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Section: Discussionmentioning

confidence: 49%

Impact of direct‐acting antiviral regimens on mortality and morbidity outcomes in patients with chronic hepatitis c: Systematic review and meta‐analysis

Sahakyan

Lee-Kim

Bremner

et al. 2021

Journal of Viral Hepatitis

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“…Finally, we demonstrated that c-MYC is involved in the mechanism underlying HBx-induced URI1 expression, and that the E-box in the URI1 promoter is a biding site for c-MYC in HCC-B (Figure 4C). Although current clinical guidelines prioritize the treatment of HCC, it is also suggested that patients with HCC-B should undergo antivirus therapy prior to HCC treatment to reduce the risks of further liver injury, HBV reactivation, and HCC recurrence [19]. Therefore, the appropriate management of chronic HBV infection in HCC is attracting attention.…”

Section: Discussionmentioning

confidence: 99%

HBx and c-MYC Cooperate to Induce URI1 Expression in HBV-Related Hepatocellular Carcinoma

Tsuchiya

Amisaki

Takenaga

et al. 2019

IJMS

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Unconventional prefoldin RNA polymerase II subunit 5 interactor (URI1) has emerged as an oncogenic driver in hepatocellular carcinoma (HCC). Although the hepatitis B virus (HBV) represents the most common etiology of HCC worldwide, it is unknown whether URI1 plays a role in HBV-related HCC (HCC-B). In the present study, we investigated URI1 expression and its underlying mechanism in HCC-B tissues and cell lines. URI1 gene-promoter activity was determined by a luciferase assay. Human HCC-B samples were used for a chromatin immunoprecipitation assay. We found that c-MYC induced URI1 expression and activated the URI1 promoter through the E-box in the promoter region while the HBx protein significantly enhanced it. The positivity of URI1 expression was significantly higher in HCC-B tumor tissues than in non-HBV-related HCC tumor tissues, suggesting that a specific mechanism underlies URI1 expression in HCC-B. In tumor tissues from HCC-B patients, a significantly higher level of c-MYC was recruited to the E-box than in non-tumor tissues. These results suggest that HBx and c-MYC are involved in URI1 expression in HCC-B. URI1 expression may play important roles in the development and progression of HCC-B because HBx and c-MYC are well-known oncogenic factors in the virus and host, respectively.

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“…IκBα is considered to be a tumor-suppressing factor in different types of cancer, such as breast (23,24), ovarian (25), gastric (26) and colorectal (27), mainly due to its inhibition of NF-κB activity; however, the underlying mechanism is yet to be elucidated. Liver tumorigenesis is usually attributed to inflammation (28). Cell proliferation increases during inflammation, in which accelerated DNA replication results in the increased occurrence of oncogenic mutation (29).…”

Section: Discussionmentioning

confidence: 99%

Reduced IκBα promotes hepatocellular carcinoma cell proliferation and migration via regulation of NF‑κB/Erbin axis

et al. 2020

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Aberrantly low expression of NF-κB inhibitor α (IκBα) is observed in hepatocellular carcinoma (HCC), yet the underlying mechanism via which IκBα regulates HCC remains largely unknown. Therefore, to determine the potential function of IκBα in hepatocarcinogenesis, the present study used immunohistochemistry (IHC) staining to analyze the associations between IκBα protein expression and clinicopathologic characteristics of 107 patients with HCC. It was found that expression of IκBα was significantly associated with tumor recurrence. Moreover, IκBα protein expression was decreased in 107 HCC tissue samples and was positively associated with overall survival. Mechanistically, it was demonstrated that silencing of IκBα activated NF-κB in both Huh7 and HCCLM3 cells, followed by upregulation of Erbb2 interacting protein (Erbin) at both the mRNA and protein levels, confirmed by reverse transcription-quantitative PCR and western blotting, to promote cell proliferation and migration. Furthermore, knockdown of Erbin significantly attenuated NF-κB-mediated cell proliferation and migration. It was also identified that overexpression of Erbin in HCC tissues promoted both cell proliferation and migration, and was negatively associated with IκBα expression in 107 HCC tissue samples. Thus, these results indicated that downregulation of IκBα promoted HCC tumorigenesis via upregulation of NF-κB-mediated Erbin expression.

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What Comes First: Treatment of Viral Hepatitis or Liver Cancer?

Cited by 12 publications

References 45 publications

Impact of direct‐acting antiviral regimens on mortality and morbidity outcomes in patients with chronic hepatitis c: Systematic review and meta‐analysis

Impact of direct‐acting antiviral regimens on mortality and morbidity outcomes in patients with chronic hepatitis c: Systematic review and meta‐analysis

HBx and c-MYC Cooperate to Induce URI1 Expression in HBV-Related Hepatocellular Carcinoma

Reduced IκBα promotes hepatocellular carcinoma cell proliferation and migration via regulation of NF‑κB/Erbin axis

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What Comes First: Treatment of Viral Hepatitis or Liver Cancer?

Cited by 12 publications

References 45 publications

Impact of direct‐acting antiviral regimens on mortality and morbidity outcomes in patients with chronic hepatitis c: Systematic review and meta‐analysis

Impact of direct‐acting antiviral regimens on mortality and morbidity outcomes in patients with chronic hepatitis c: Systematic review and meta‐analysis

HBx and c-MYC Cooperate to Induce URI1 Expression in HBV-Related Hepatocellular Carcinoma

Reduced I&kappa;B&alpha; promotes hepatocellular carcinoma cell proliferation and migration via regulation of NF‑&kappa;B/Erbin axis

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Reduced IκBα promotes hepatocellular carcinoma cell proliferation and migration via regulation of NF‑κB/Erbin axis