Letter to the Editor: Tenofovir vs. Entecavir on Recurrence of Hepatitis B Virus–Related Hepatocellular Carcinoma After Surgical Resection

Yuan, Guandou; Yao, Jianni; Yu, Jingjing; Xie, Xuemei; He, Songqing

doi:10.1002/hep.31590

Cited by 3 publications

(3 citation statements)

References 6 publications

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“…In one study by Wong [ 15 ], NA therapy was associated with a 41% reduction in the risk of HCC recurrence after curative treatment of HCC and was associated with a 90% reduction in the risk of liver-related mortality and 78% reduction in overall mortality. Comparable findings were reported by other groups and confirmed that antiviral therapy with NA is independently protective of both early and late recurrence of HCC after treatments [ 105 ]. Importantly, antiviral therapy with NA was independently associated with improved survival also in patients receiving non-curative treatment, such as chemoembolization [ 106 , 107 , 108 ].…”

Section: The Impact Of Antiviral Therapy On the Risk Of Hcc In Patients With Chronic Viral Infectionsupporting

confidence: 87%

Hepatocellular Carcinoma in Chronic Viral Hepatitis: Where Do We Stand?

Russo

Zanetto

Pinto

et al. 2022

IJMS

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Hepatocellular carcinoma (HCC) is one of the major causes of cancer-related death. Although the burden of alcohol- and NASH-related HCC is growing, chronic viral hepatitis (HBV and HCV) remains a major cause of HCC development worldwide. The pathophysiology of viral-related HCC includes liver inflammation, oxidative stress, and deregulation of cell signaling pathways. HBV is particularly oncogenic because, contrary to HCV, integrates in the cell DNA and persists despite virological suppression by nucleotide analogues. Surveillance by six-month ultrasound is recommended in patients with cirrhosis and in “high-risk” patients with chronic HBV infection. Antiviral therapy reduces the risks of development and recurrence of HCC; however, patients with advanced chronic liver disease remain at risk of HCC despite virological suppression/cure and should therefore continue surveillance. Multiple scores have been developed in patients with chronic hepatitis B to predict the risk of HCC development and may be used to stratify individual patient’s risk. In patients with HCV-related liver disease who achieve sustained virological response by direct acting antivirals, there is a strong need for markers/scores to predict long-term risk of HCC. In this review, we discuss the most recent advances regarding viral-related HCC.

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Section: The Impact Of Antiviral Therapy On the Risk Of Hcc In Patients With Chronic Viral Infectionsupporting

confidence: 87%

Hepatocellular Carcinoma in Chronic Viral Hepatitis: Where Do We Stand?

Russo

Zanetto

Pinto

et al. 2022

IJMS

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“…11,12 However, clinical practices attested to the unfavorable status of HBV-HCC patients who received antiviral therapy before surgery. [13][14][15] The urgent need for HBV-HCC treatment optimization is broadly recognized.…”

Section: Introductionmentioning

confidence: 99%

“…Data from several studies illustrated that high viral load or HBV reactivation was linked to a high risk of HCC relapse, demonstrating the potential utility of antiviral therapy in HCC relapse 11,12 . However, clinical practices attested to the unfavorable status of HBV‐HCC patients who received antiviral therapy before surgery 13–15 . The urgent need for HBV‐HCC treatment optimization is broadly recognized.…”

Section: Introductionmentioning

confidence: 99%

Novel insights into HBV‐hepatocellular carcinoma at single‐cell sequencing

Yin,

Zhou,

Xia

et al. 2023

MedComm – Oncology

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A significant proportion of hepatocellular carcinoma (HCC) is pathologically associated with hepatitis B virus (HBV) infection, followed by unsatisfied clinical outcomes. The increasing unmet need for HBV‐associated hepatocellular carcinoma (HBV‐HCC) treatment drives to deeper understand the role of the intricate immune microenvironment, tumor cell plasticity and dynamics of tumor evolution in HBV‐associated hepatic carcinogenesis. Thus, a comprehensive understanding of cross‐talk between HBV, host cells, and tumor microenvironment is of fundamental importance for identifying immune imbalance and heterogeneity in HBV‐HCC. Over the past 5 years, the application of single‐cell RNA sequencing (scRNA‐seq) in the understanding of heterogeneity and dynamics of immune cells, clonal evolution, and cancer stem cell (CSC) subsets of tumor cells has established a landscape for HBV‐HCC tumor ecosystem. Novel insights into anatomizing immune escape mechanisms and tumor drug resistance have remarkably facilitated the revolution of HBV‐HCC clinical treatment. Here, we provided a summary of HCC at single‐cell resolution and details on the basic workflow, limitations, and improvements of scRNA‐seq. The review highlights novel insights derived from scRNA‐seq on advances in the immune microenvironment and tumor heterogeneity of HBV‐HCC.

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RBM15 promotes hepatocellular carcinoma progression by regulating N6-methyladenosine modification of YES1 mRNA in an IGF2BP1-dependent manner

et al. 2021

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The function of the N6-methyladenosine (m6A) methyltransferase RNA-binding motif protein 15 (RBM15) in hepatocellular carcinoma (HCC) has not been thoroughly investigated. Here we determined the clinical value, biological functions, and potential mechanisms of RBM15 in HCC. Expression of RBM15 was identified using tissue microarrays and online databases. A risk-prediction model based on RBM15 was developed and validated. We determined the biological role of RBM15 on HCC cells in vitro and in vivo. RNA sequencing was used to screen candidate targets of RBM15. Subsequently, the m6A dot blot assay, methylated RNA immunoprecipitation qPCR, dual-luciferase reporter assays, RNA decay assay, and RNA immunoprecipitation qPCR were employed to explore the mechanisms of RBM15. Our study showed that RBM15 was highly expressed in HCC, and overexpression of RBM15 indicated a worse outcome. A new nomogram combining RBM15 with age and TNM stage was developed and validated to predict the outcome of HCC patients; our nomogram increased the prediction accuracy of the TNM system. Functionally, RBM15 facilitates the proliferation and invasiveness of HCC. RBM15-mediated m6A modification contributed to a post-transcriptional activation of YES proto-oncogene 1 (YES1) in an insulin-like growth factor 2 mRNA-binding protein 1 (IGF2BP1)-dependent manner. In addition, YES1 was confirmed as an oncogene in HCC cells by activating the mitogen-activated protein kinase (MAPK) pathway. In conclusion, RBM15-mediated m6A modification might facilitate the progression of HCC via the IGF2BP1–YES1–MAPK axis. RBM15 may be a promising biomarker in the outcome prediction of HCC.

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Letter to the Editor: Tenofovir vs. Entecavir on Recurrence of Hepatitis B Virus–Related Hepatocellular Carcinoma After Surgical Resection

Cited by 3 publications

References 6 publications

Hepatocellular Carcinoma in Chronic Viral Hepatitis: Where Do We Stand?

Hepatocellular Carcinoma in Chronic Viral Hepatitis: Where Do We Stand?

Novel insights into HBV‐hepatocellular carcinoma at single‐cell sequencing

RBM15 promotes hepatocellular carcinoma progression by regulating N6-methyladenosine modification of YES1 mRNA in an IGF2BP1-dependent manner

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